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"content": "\u003cp>Once again, COVID-19 has not taken a summer vacation.\u003c/p>\n\u003cp>\u003ca href=\"https://data.wastewaterscan.org/\">Wastewater measurements\u003c/a> reveal a swell in virus levels across the Bay Area and the state.\u003c/p>\n\u003cp>\u003ca href=\"https://www.kqed.org/news/11957790/the-new-covid-eris-variant-and-rising-cases-what-you-need-to-know\">“Eris,” or EG.5 is the dominant strain in the U.S. right now\u003c/a> and is driving the local activity, too. The variant does not seem to be any more dangerous than previous variants, but it is more transmissible.\u003c/p>\n\u003cp>“The interesting thing is: COVID hasn’t really changed too much, since winter to now,” said Peter Chin-Hong, infectious disease specialist at UCSF. “It’s just been variations on the theme.”\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>That could be changing. A subvariant that’s just beginning to surface may be the best yet at evading immunity. Scientists for the Centers for Disease and Prevention are watching \u003ca href=\"https://www.cdc.gov/respiratory-viruses/whats-new/covid-19-variant.html\" target=\"_blank\" rel=\"noopener\">BA.286\u003c/a> because it has even greater potential to escape the antibodies that protect people from getting sick, even if you’ve recently tested positive or been vaccinated. It is too early to know if it causes more serious illness. There are only a handful of cases in the U.S.\u003c/p>\n\u003cp>This is the fourth summer in a row that COVID-19 has spread rapidly in California. Health experts offer several explanations for the recent uptick. People may be seeking relief from scorching temperatures by staying inside air-conditioned spaces. For most folks life is back to normal, so large gatherings have resumed in full force. And, immunity may be declining because the last vaccine campaign was in the fall.\u003c/p>\n\u003cp>All of these factors, in addition to a wily virus, are likely why scientists are not seeing a predictable seasonal pattern like influenza, which typically strikes when it’s cold. It’s not clear when COVID-19 will settle into an annual surge.\u003c/p>\n\u003cp>“I’d hope it would be a once-a-year virus,” said Chin-Hong. “But it just seems that the summer increase in cases is something that we continue to see.”\u003c/p>\n\u003cp>Virus levels are still lower than earlier surges. And it’s worth noting that the wastewater data is pretty noisy.[aside label=\"Related Stories\" postID=\"science_1984081,news_11957790,forum_2010101894165\"]At a sewage plant in Redwood City, levels are spiking, but declining in San Francisco’s Oceanside neighborhood and falling dramatically at similar facilities in Sunnyvale and Palo Alto.\u003c/p>\n\u003cp>Los Angeles is seeing a slow rise, while virus levels started to slowly fall off in Sacramento recently.\u003c/p>\n\u003cp>Given the current numbers, Chin-Hong does recommend taking additional precautions. He suggested people who are immunocompromised and those over the age of 65 consider masking indoors, given their higher susceptibility to severe illness.\u003c/p>\n\u003cp>Everyone else may want to weigh the consequences of falling ill at this time. Can you miss work? Do you have a special occasion on the books that you’d have to miss if you were isolated for five days, which public health officials still recommend people do after a positive test? Then it may be a good time to err on the safe side if you don’t want to end up at home alone. You could carry your well-fitting N95 mask in case you find yourself in a crowded indoor space.\u003c/p>\n\u003cp>The public will have the opportunity to fortify immunity soon. A new booster shot will likely be available in late September, designed to target the variants in wide circulation now.\u003c/p>\n\u003cp>Feeling like a pin cushion? There’s good news for those suffering from booster fatigue. Scientists are working on a \u003ca href=\"https://www.nih.gov/news-events/nih-research-matters/research-context-progress-toward-universal-vaccines\" target=\"_blank\" rel=\"noopener\">universal vaccine\u003c/a>, which, in theory, would allow one-stop shopping. Unlike current vaccines, which offer protection against one or several strains of a disease, universal vaccines are designed to teach the immune system to defend against all versions of a pathogen — even versions that don’t exist yet. This is possible by targeting an element of the pathogen that is the same across all strains and types.\u003c/p>\n\u003cp>“That is the holy grail,” said Chin-Hong. “I think we will probably get something in the next two-to-three years. They are also working on that for influenza.”\u003c/p>\n\u003cp>In the meantime, he says, we could see a combination vaccine that provides protection for COVID-19 and influenza as early as next year.\u003c/p>\n\u003cp> \u003c/p>\n\u003cp> \u003c/p>\n\u003cp> \u003c/p>\n\u003cp>\u003c/p>\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>That could be changing. A subvariant that’s just beginning to surface may be the best yet at evading immunity. Scientists for the Centers for Disease and Prevention are watching \u003ca href=\"https://www.cdc.gov/respiratory-viruses/whats-new/covid-19-variant.html\" target=\"_blank\" rel=\"noopener\">BA.286\u003c/a> because it has even greater potential to escape the antibodies that protect people from getting sick, even if you’ve recently tested positive or been vaccinated. It is too early to know if it causes more serious illness. There are only a handful of cases in the U.S.\u003c/p>\n\u003cp>This is the fourth summer in a row that COVID-19 has spread rapidly in California. Health experts offer several explanations for the recent uptick. People may be seeking relief from scorching temperatures by staying inside air-conditioned spaces. For most folks life is back to normal, so large gatherings have resumed in full force. And, immunity may be declining because the last vaccine campaign was in the fall.\u003c/p>\n\u003cp>All of these factors, in addition to a wily virus, are likely why scientists are not seeing a predictable seasonal pattern like influenza, which typically strikes when it’s cold. It’s not clear when COVID-19 will settle into an annual surge.\u003c/p>\n\u003cp>“I’d hope it would be a once-a-year virus,” said Chin-Hong. “But it just seems that the summer increase in cases is something that we continue to see.”\u003c/p>\n\u003cp>Virus levels are still lower than earlier surges. And it’s worth noting that the wastewater data is pretty noisy.\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>At a sewage plant in Redwood City, levels are spiking, but declining in San Francisco’s Oceanside neighborhood and falling dramatically at similar facilities in Sunnyvale and Palo Alto.\u003c/p>\n\u003cp>Los Angeles is seeing a slow rise, while virus levels started to slowly fall off in Sacramento recently.\u003c/p>\n\u003cp>Given the current numbers, Chin-Hong does recommend taking additional precautions. He suggested people who are immunocompromised and those over the age of 65 consider masking indoors, given their higher susceptibility to severe illness.\u003c/p>\n\u003cp>Everyone else may want to weigh the consequences of falling ill at this time. Can you miss work? Do you have a special occasion on the books that you’d have to miss if you were isolated for five days, which public health officials still recommend people do after a positive test? Then it may be a good time to err on the safe side if you don’t want to end up at home alone. You could carry your well-fitting N95 mask in case you find yourself in a crowded indoor space.\u003c/p>\n\u003cp>The public will have the opportunity to fortify immunity soon. A new booster shot will likely be available in late September, designed to target the variants in wide circulation now.\u003c/p>\n\u003cp>Feeling like a pin cushion? There’s good news for those suffering from booster fatigue. Scientists are working on a \u003ca href=\"https://www.nih.gov/news-events/nih-research-matters/research-context-progress-toward-universal-vaccines\" target=\"_blank\" rel=\"noopener\">universal vaccine\u003c/a>, which, in theory, would allow one-stop shopping. Unlike current vaccines, which offer protection against one or several strains of a disease, universal vaccines are designed to teach the immune system to defend against all versions of a pathogen — even versions that don’t exist yet. This is possible by targeting an element of the pathogen that is the same across all strains and types.\u003c/p>\n\u003cp>“That is the holy grail,” said Chin-Hong. “I think we will probably get something in the next two-to-three years. They are also working on that for influenza.”\u003c/p>\n\u003cp>In the meantime, he says, we could see a combination vaccine that provides protection for COVID-19 and influenza as early as next year.\u003c/p>\n\u003cp> \u003c/p>\n\u003cp> \u003c/p>\n\u003cp> \u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>",
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"title": "COVID-19, a Disease With Tricks Up Its Sleeve, Hasn’t Fallen Into a Seasonal Pattern — Yet",
"headTitle": "COVID-19, a Disease With Tricks Up Its Sleeve, Hasn’t Fallen Into a Seasonal Pattern — Yet | KQED",
"content": "\u003cp>To most people on the planet, the COVID-19 pandemic is over. But for many scientists who have been tracking the largest global infectious disease event in the era of molecular biology, there is still a step that the virus that caused it, SARS-CoV-2, hasn’t yet taken. It has not fallen into a predictable seasonal pattern of the type most respiratory pathogens follow.\u003c/p>\n\u003cp>Influenza strikes — at least in temperate climates — in the winter months, with activity often peaking in January or February. In the pre-COVID times, that was also true for RSV — respiratory syncytial virus — and a number of other bugs that inflict cold- and flu-like illnesses. Some respiratory pathogens seem to prefer fall or spring. Even measles, when that disease circulated widely, had a seasonality in our part of the world, typically striking in late winter or early spring.\u003c/p>\n\u003cp>To be sure, you can contract these viruses at any time of the year. But transmission takes off during a particular pathogen’s season. (The COVID pandemic knocked a number of these bugs \u003ca href=\"https://www.statnews.com/2022/05/25/viruses-that-were-on-hiatus-during-covid-are-back-and-behaving-in-unexpected-ways/\">out of their regular orbits\u003c/a>, though they may be heading back to more normal transmission patterns. The next few months should be telling.)\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>It’s been widely expected that SARS-2 will ease into that type of a transmission pattern, once human immune systems and the virus reach a sort of detente. But most experts STAT spoke to about this question said that, so far, the virus has not obliged. Their views differ on the margins. Some expect seasonality to set in soon while others don’t venture to guess when the virus will settle into a seasonal pattern.\u003c/p>\n\u003cp>“I don’t see clear seasonality for SARS-CoV-2 yet,” Kanta Subbarao, director of the World Health Organization’s Collaborating Centre for Reference and Research on Influenza at the Peter Doherty Institute for Infection and Immunity in Melbourne, Australia, said via email. Subbarao is also chair of the WHO’s technical advisory group on COVID-19 vaccine composition, an independent panel that recommends which version or versions of SARS-2 should be included in updated COVID vaccines.\u003c/p>\n\u003cp>Michael Osterholm, director of the University of Minnesota’s Center for Infectious Disease Research and Policy, agreed. “There just isn’t a definable pattern yet that would call this a seasonal virus. That’s not to suggest it might not be some day.”[pullquote align=\"right\" size=\"medium\" citation=\"Ben Cowling, infectious diseases epidemiologist, University of Hong Kong\"]‘At the moment I don’t think COVID is predictable but it is showing all the signs of becoming the fifth ‘human coronavirus’ along with OC43, NL63, 229E and HKU1.’[/pullquote]Maria Van Kerkhove, the WHO’s technical lead for COVID, told STAT in a recent interview that the lack of seasonality is clear. “We expect there to be some seasonality in the coming years. Just based on people’s behavior, perhaps, just because it’s respiratory,” she said. Van Kerkhove does, though, think there are hints of a transmission pattern that is coming into view, something she and others refer to as “periodicity.”\u003c/p>\n\u003cp>“If you kind of squint, you could see a little, you know, in different places,” Van Kerkhove said. “I think you can see sort of waves of infection every five, six months or so depending on the population. But that isn’t at a national level. … And it’s not hemispheric.”\u003c/p>\n\u003cp>Questions posed over SARS-2’s lack of seasonality aren’t purely academic. Knowing when to expect a disease is critical for health care labor force planning. The tsunami of RSV-infected babies struggling to breathe in the late summer and early fall of 2022 was made worse by the fact that hospitals weren’t as prepared as they could have been; they normally see RSV peaks in the winter months. Likewise, knowing when to expect SARS-2 surges helps the Food and Drug Administration and the Centers for Disease Control and Prevention time the rollout of COVID booster shots. The protection against infection generated by the vaccines wanes quickly, so giving them too soon or too late would undermine the efficacy of this countermeasure.\u003c/p>\n\u003cp>Van Kerkhove thinks waning immunity in the population is the reason for the periodic swells of transmission. Protection against severe disease — whether induced by infection, vaccination, or the two combined — appears to hold up reasonably well. But when it comes to SARS-2, protection against basic infection is short-lived. That’s not a surprise given what’s known about the four human coronaviruses that predate the arrival of SARS-2. A study in the Netherlands that followed healthy volunteers for more than 35 years found that people can be reinfected with human coronaviruses within about a year after infection, and sometimes after a mere six months. With SARS-2, there are reports of intervals that are shorter still.\u003c/p>\n\u003cp>Michael Mina, an infectious diseases epidemiologist who previously taught at the Harvard School of Public Health, is a bit of an outlier in this conversation. He believes SARS-2 has been displaying seasonal behavior for a while, though what he describes sounds like the periodicity that Van Kerkhove and some other experts speak of.\u003c/p>\n\u003cp>Mina thinks of seasonality in terms of predictability, “that certain periods of time are going to see increases and decreases, but not necessarily that it has to just be winter or summer.”\u003c/p>\n\u003cp>“I don’t think I use the word wrong but I don’t think it’s well defined one way or the other,” he noted.[aside label=\"Related Stories\" postID=\"news_11957790,news_11954507,forum_2010101894165\"]Ben Cowling, an infectious diseases epidemiologist at the University of Hong Kong, also thinks seasonality and predictability are intertwined. He doesn’t think SARS-2 is there yet — but believes it’s on its way.\u003c/p>\n\u003cp>“At the moment I don’t think COVID is predictable but it is showing all the signs of becoming the fifth ‘human coronavirus’ along with OC43, NL63, 229E and HKU1,” he said in an email, ticking off the names of the four human coronaviruses that predated SARS-2.\u003c/p>\n\u003cp>Osterholm doesn’t agree, arguing that even if they follow a pattern, swells of COVID cases at different points in a year doesn’t equate to seasonality. Furthermore, he noted that the patterns we’ve seen to date have been largely tied to the emergence of new variants, like Beta, Delta, and Omicron, with large surges of infections when those versions of SARS-2 arrived in the spring, summer, and late autumn of 2021 respectively.\u003c/p>\n\u003cp>“It wasn’t tied to some kind of environmental conditions. And that’s what you often think of with seasonality,” Osterholm said.\u003c/p>\n\u003cp>It’s thought that with new viruses, the vast number of susceptible people allows a virus to override conditions that would constrain more established pathogens — kids being out of school, unfavorable atmospheric conditions — and transmit at a time when it normally should not be able to. Epidemiologists refer to this override capacity as the “force of infection.”\u003c/p>\n\u003cp>That, in turn, can impact the ability of other pathogens to transmit during their accustomed times, as was the case with COVID’s disruption of flu and RSV. “When a virus is in a pandemic mode, there are forces occurring that we just don’t understand,” Osterholm said.\u003c/p>\n\u003cp>There are a number of theories about why some viruses hew to a seasonal pattern. It’s thought an interplay of factors is at work. Some have been mapped out, others remain in the realm of the unexplained.\u003c/p>\n\u003cp>Some relate to human activities, like school, that bring together lots of children, who are \u003ca href=\"https://www.statnews.com/2020/02/27/coronavirus-kids-what-role-transmission/\">expert at amplifying\u003c/a> respiratory pathogens. Or holiday travel, potentially. Marion Koopmans, head of virology at Erasmus Medical Center in Rotterdam, the Netherlands, noted that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8324533/\">a study\u003c/a> published in Nature suggested that a surge in Covid cases in the summer of 2020 in Europe was likely due to people vacationing. “Without detailed analysis, I do not think we can rule out that what we see is ‘holiday traffic,’” Koopmans said, referring to the upticks of cases that have been reported every Northern Hemisphere summer since 2020.\u003c/p>\n\u003cp>Environmental factors are also thought to be at play. The lack of humidity in the air in cold winters affects the integrity of mucus membranes, and it allows viruses to \u003ca href=\"https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003194\">survive better\u003c/a> outside a human host. People in temperate climates crowd together indoors during the winter, often in settings where air quality is suboptimal. Interestingly, the defined flu seasons that the Northern and Southern Hemispheres experience are not observed in tropical climates, where transmission occurs on a more \u003ca href=\"https://www.embopress.org/doi/full/10.15252/emmm.202115352\">year-round basis\u003c/a>, without the sharp peaks seen in temperate zones.\u003c/p>\n\u003cp>“There is now a much stronger evidence base on the impact of climate variables (esp. temperature, humidity) on pathogen survival and how this translates to an impact on transmission in the population,” Nick Grassly, an infectious diseases modeler at the school of public health at Imperial College London, said in an email. “The focus has been much more on environmental drivers (particularly humidity, temperature, rainfall, etc.) than human behavior.”\u003c/p>\n\u003cp>Grassly is one of the people who thinks SARS-2 seasonality is falling into place, noting that the Joint Committee on Vaccination and Immunisation — Britain’s equivalent of the Advisory Committee on Immunization Practices, an expert committee that helps the CDC craft vaccination use guidelines — is now recommending a targeted \u003ca href=\"https://www.gov.uk/government/news/jcvi-advises-an-autumn-covid-19-vaccine-booster\">autumn COVID vaccination campaign\u003c/a> for high-risk individuals, in anticipation of a surge of COVID activity this winter. A similar, though more broadly aimed campaign is planned for the United States.\u003c/p>\n\u003cp>“It remains possible that a new variant showing substantial immune escape could spread rapidly, even in summer, and so disrupt seasonal patterns and planning,” Grassly noted. “I think it is hard to estimate the probability that this happens, but it would deviate from the recent pattern of successive Omicron variants which have emerged without large increases in overall incidence.”\u003c/p>\n\u003cp>Stanley Perlman, a coronavirus expert whose bona fides in the field stretch back to the pre-SARS-1 days, agrees with Grassly.[pullquote align=\"right\" size=\"medium\" citation=\"Marion Koopmans, head of virology, Erasmus Medical Center\"]‘I think that — at this stage — all we can say is that we can assume that there are some seasonal effects … but that we really cannot say the circulation of these viruses is predictable yet, at least not like we have come to know for flu.’[/pullquote]“I think for all these viruses” — human coronaviruses — “they probably circulate all year round. But you get large numbers of infections in the late fall, winter, when people are inside, and they spread. That’s what this virus seems to be doing,” said Perlman, a professor of microbiology and immunology at the University of Iowa. “As opposed to last summer, the number of cases is way down this summer. And the prediction is they will increase in the late fall, winter again.”\u003c/p>\n\u003cp>A break from seasonal transmission of respiratory pathogens can be a sign something is amiss, with off-season spread having been observed during flu pandemics going back to the Spanish flu pandemic of 1918. The first observed cases in that pandemic occurred in the spring, at a time when flu season would normally have concluded. The 1957 pandemic began in Asia in February of that year, but the virus arrived in, and started spreading through, the United States, during the summer. The 1968 pandemic began in July. The 2009 H1N1 pandemic was first detected in April and the pandemic’s major wave ran through the summer, peaked in September and trailed off in October.\u003c/p>\n\u003cp>“Pandemic influenza doesn’t follow a seasonal pattern in any way, shape or form,” said Osterholm.\u003c/p>\n\u003cp>It remains to be seen when it will be apparent that SARS-2 has lost its override capabilities, when we’ll feel confident that we know when to expect — plus or minus a month or two — COVID’s annual onslaught.\u003c/p>\n\u003cp>“I think that — at this stage — all we can say is that we can assume that there are some seasonal effects (since we know seasonality does have an effect on other respiratory infections, both by effects on virus stability and on the host) but that we really cannot say the circulation of these viruses is predictable yet, at least not like we have come to know for flu,” Koopmans wrote.\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>To most people on the planet, the COVID-19 pandemic is over. But for many scientists who have been tracking the largest global infectious disease event in the era of molecular biology, there is still a step that the virus that caused it, SARS-CoV-2, hasn’t yet taken. It has not fallen into a predictable seasonal pattern of the type most respiratory pathogens follow.\u003c/p>\n\u003cp>Influenza strikes — at least in temperate climates — in the winter months, with activity often peaking in January or February. In the pre-COVID times, that was also true for RSV — respiratory syncytial virus — and a number of other bugs that inflict cold- and flu-like illnesses. Some respiratory pathogens seem to prefer fall or spring. Even measles, when that disease circulated widely, had a seasonality in our part of the world, typically striking in late winter or early spring.\u003c/p>\n\u003cp>To be sure, you can contract these viruses at any time of the year. But transmission takes off during a particular pathogen’s season. (The COVID pandemic knocked a number of these bugs \u003ca href=\"https://www.statnews.com/2022/05/25/viruses-that-were-on-hiatus-during-covid-are-back-and-behaving-in-unexpected-ways/\">out of their regular orbits\u003c/a>, though they may be heading back to more normal transmission patterns. The next few months should be telling.)\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>It’s been widely expected that SARS-2 will ease into that type of a transmission pattern, once human immune systems and the virus reach a sort of detente. But most experts STAT spoke to about this question said that, so far, the virus has not obliged. Their views differ on the margins. Some expect seasonality to set in soon while others don’t venture to guess when the virus will settle into a seasonal pattern.\u003c/p>\n\u003cp>“I don’t see clear seasonality for SARS-CoV-2 yet,” Kanta Subbarao, director of the World Health Organization’s Collaborating Centre for Reference and Research on Influenza at the Peter Doherty Institute for Infection and Immunity in Melbourne, Australia, said via email. Subbarao is also chair of the WHO’s technical advisory group on COVID-19 vaccine composition, an independent panel that recommends which version or versions of SARS-2 should be included in updated COVID vaccines.\u003c/p>\n\u003cp>Michael Osterholm, director of the University of Minnesota’s Center for Infectious Disease Research and Policy, agreed. “There just isn’t a definable pattern yet that would call this a seasonal virus. That’s not to suggest it might not be some day.”\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>Maria Van Kerkhove, the WHO’s technical lead for COVID, told STAT in a recent interview that the lack of seasonality is clear. “We expect there to be some seasonality in the coming years. Just based on people’s behavior, perhaps, just because it’s respiratory,” she said. Van Kerkhove does, though, think there are hints of a transmission pattern that is coming into view, something she and others refer to as “periodicity.”\u003c/p>\n\u003cp>“If you kind of squint, you could see a little, you know, in different places,” Van Kerkhove said. “I think you can see sort of waves of infection every five, six months or so depending on the population. But that isn’t at a national level. … And it’s not hemispheric.”\u003c/p>\n\u003cp>Questions posed over SARS-2’s lack of seasonality aren’t purely academic. Knowing when to expect a disease is critical for health care labor force planning. The tsunami of RSV-infected babies struggling to breathe in the late summer and early fall of 2022 was made worse by the fact that hospitals weren’t as prepared as they could have been; they normally see RSV peaks in the winter months. Likewise, knowing when to expect SARS-2 surges helps the Food and Drug Administration and the Centers for Disease Control and Prevention time the rollout of COVID booster shots. The protection against infection generated by the vaccines wanes quickly, so giving them too soon or too late would undermine the efficacy of this countermeasure.\u003c/p>\n\u003cp>Van Kerkhove thinks waning immunity in the population is the reason for the periodic swells of transmission. Protection against severe disease — whether induced by infection, vaccination, or the two combined — appears to hold up reasonably well. But when it comes to SARS-2, protection against basic infection is short-lived. That’s not a surprise given what’s known about the four human coronaviruses that predate the arrival of SARS-2. A study in the Netherlands that followed healthy volunteers for more than 35 years found that people can be reinfected with human coronaviruses within about a year after infection, and sometimes after a mere six months. With SARS-2, there are reports of intervals that are shorter still.\u003c/p>\n\u003cp>Michael Mina, an infectious diseases epidemiologist who previously taught at the Harvard School of Public Health, is a bit of an outlier in this conversation. He believes SARS-2 has been displaying seasonal behavior for a while, though what he describes sounds like the periodicity that Van Kerkhove and some other experts speak of.\u003c/p>\n\u003cp>Mina thinks of seasonality in terms of predictability, “that certain periods of time are going to see increases and decreases, but not necessarily that it has to just be winter or summer.”\u003c/p>\n\u003cp>“I don’t think I use the word wrong but I don’t think it’s well defined one way or the other,” he noted.\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>Ben Cowling, an infectious diseases epidemiologist at the University of Hong Kong, also thinks seasonality and predictability are intertwined. He doesn’t think SARS-2 is there yet — but believes it’s on its way.\u003c/p>\n\u003cp>“At the moment I don’t think COVID is predictable but it is showing all the signs of becoming the fifth ‘human coronavirus’ along with OC43, NL63, 229E and HKU1,” he said in an email, ticking off the names of the four human coronaviruses that predated SARS-2.\u003c/p>\n\u003cp>Osterholm doesn’t agree, arguing that even if they follow a pattern, swells of COVID cases at different points in a year doesn’t equate to seasonality. Furthermore, he noted that the patterns we’ve seen to date have been largely tied to the emergence of new variants, like Beta, Delta, and Omicron, with large surges of infections when those versions of SARS-2 arrived in the spring, summer, and late autumn of 2021 respectively.\u003c/p>\n\u003cp>“It wasn’t tied to some kind of environmental conditions. And that’s what you often think of with seasonality,” Osterholm said.\u003c/p>\n\u003cp>It’s thought that with new viruses, the vast number of susceptible people allows a virus to override conditions that would constrain more established pathogens — kids being out of school, unfavorable atmospheric conditions — and transmit at a time when it normally should not be able to. Epidemiologists refer to this override capacity as the “force of infection.”\u003c/p>\n\u003cp>That, in turn, can impact the ability of other pathogens to transmit during their accustomed times, as was the case with COVID’s disruption of flu and RSV. “When a virus is in a pandemic mode, there are forces occurring that we just don’t understand,” Osterholm said.\u003c/p>\n\u003cp>There are a number of theories about why some viruses hew to a seasonal pattern. It’s thought an interplay of factors is at work. Some have been mapped out, others remain in the realm of the unexplained.\u003c/p>\n\u003cp>Some relate to human activities, like school, that bring together lots of children, who are \u003ca href=\"https://www.statnews.com/2020/02/27/coronavirus-kids-what-role-transmission/\">expert at amplifying\u003c/a> respiratory pathogens. Or holiday travel, potentially. Marion Koopmans, head of virology at Erasmus Medical Center in Rotterdam, the Netherlands, noted that \u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8324533/\">a study\u003c/a> published in Nature suggested that a surge in Covid cases in the summer of 2020 in Europe was likely due to people vacationing. “Without detailed analysis, I do not think we can rule out that what we see is ‘holiday traffic,’” Koopmans said, referring to the upticks of cases that have been reported every Northern Hemisphere summer since 2020.\u003c/p>\n\u003cp>Environmental factors are also thought to be at play. The lack of humidity in the air in cold winters affects the integrity of mucus membranes, and it allows viruses to \u003ca href=\"https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1003194\">survive better\u003c/a> outside a human host. People in temperate climates crowd together indoors during the winter, often in settings where air quality is suboptimal. Interestingly, the defined flu seasons that the Northern and Southern Hemispheres experience are not observed in tropical climates, where transmission occurs on a more \u003ca href=\"https://www.embopress.org/doi/full/10.15252/emmm.202115352\">year-round basis\u003c/a>, without the sharp peaks seen in temperate zones.\u003c/p>\n\u003cp>“There is now a much stronger evidence base on the impact of climate variables (esp. temperature, humidity) on pathogen survival and how this translates to an impact on transmission in the population,” Nick Grassly, an infectious diseases modeler at the school of public health at Imperial College London, said in an email. “The focus has been much more on environmental drivers (particularly humidity, temperature, rainfall, etc.) than human behavior.”\u003c/p>\n\u003cp>Grassly is one of the people who thinks SARS-2 seasonality is falling into place, noting that the Joint Committee on Vaccination and Immunisation — Britain’s equivalent of the Advisory Committee on Immunization Practices, an expert committee that helps the CDC craft vaccination use guidelines — is now recommending a targeted \u003ca href=\"https://www.gov.uk/government/news/jcvi-advises-an-autumn-covid-19-vaccine-booster\">autumn COVID vaccination campaign\u003c/a> for high-risk individuals, in anticipation of a surge of COVID activity this winter. A similar, though more broadly aimed campaign is planned for the United States.\u003c/p>\n\u003cp>“It remains possible that a new variant showing substantial immune escape could spread rapidly, even in summer, and so disrupt seasonal patterns and planning,” Grassly noted. “I think it is hard to estimate the probability that this happens, but it would deviate from the recent pattern of successive Omicron variants which have emerged without large increases in overall incidence.”\u003c/p>\n\u003cp>Stanley Perlman, a coronavirus expert whose bona fides in the field stretch back to the pre-SARS-1 days, agrees with Grassly.\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>“I think for all these viruses” — human coronaviruses — “they probably circulate all year round. But you get large numbers of infections in the late fall, winter, when people are inside, and they spread. That’s what this virus seems to be doing,” said Perlman, a professor of microbiology and immunology at the University of Iowa. “As opposed to last summer, the number of cases is way down this summer. And the prediction is they will increase in the late fall, winter again.”\u003c/p>\n\u003cp>A break from seasonal transmission of respiratory pathogens can be a sign something is amiss, with off-season spread having been observed during flu pandemics going back to the Spanish flu pandemic of 1918. The first observed cases in that pandemic occurred in the spring, at a time when flu season would normally have concluded. The 1957 pandemic began in Asia in February of that year, but the virus arrived in, and started spreading through, the United States, during the summer. The 1968 pandemic began in July. The 2009 H1N1 pandemic was first detected in April and the pandemic’s major wave ran through the summer, peaked in September and trailed off in October.\u003c/p>\n\u003cp>“Pandemic influenza doesn’t follow a seasonal pattern in any way, shape or form,” said Osterholm.\u003c/p>\n\u003cp>It remains to be seen when it will be apparent that SARS-2 has lost its override capabilities, when we’ll feel confident that we know when to expect — plus or minus a month or two — COVID’s annual onslaught.\u003c/p>\n\u003cp>“I think that — at this stage — all we can say is that we can assume that there are some seasonal effects (since we know seasonality does have an effect on other respiratory infections, both by effects on virus stability and on the host) but that we really cannot say the circulation of these viruses is predictable yet, at least not like we have come to know for flu,” Koopmans wrote.\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"title": "The Omicron Subvariant BA.2 Has Been in the Bay Area for Weeks — With Limited Impact",
"headTitle": "The Omicron Subvariant BA.2 Has Been in the Bay Area for Weeks — With Limited Impact | KQED",
"content": "\u003cp>We’ve seen this play out before: Just as we start letting down our guard, the coronavirus mutates into another insidious version, wreaking havoc on our plans.\u003c/p>\n\u003cp>Cue BA.2, or \u003ca href=\"https://www.ama-assn.org/delivering-care/public-health/what-ba2-or-stealth-omicron-subvariant\">stealth omicron\u003c/a>.\u003c/p>\n\u003cp>Earlier this month when mask mandates started falling away, the subvariant struck parts of Europe and Asia, driving \u003ca href=\"https://www.cnbc.com/2022/03/23/omicrons-subvariant-bapoint2-could-spread-wildly-in-europe-epidemiologist.html\">unprecedented spikes\u003c/a>. Now, it’s traveling fast within the U.S.\u003c/p>\n\u003cp>BA.2 is both the dominant strain globally and, now, nationally, according to the \u003ca href=\"https://covid.cdc.gov/covid-data-tracker/#variant-proportions\" target=\"_blank\" rel=\"noopener noreferrer\">Centers for Disease Control and Prevention\u003c/a>, which credits more than half of U.S. cases to stealth omicron. Infections are edging up in parts of the Northeast, and \u003ca href=\"https://soe-wbe-pilot.wl.r.appspot.com/charts#page=overview\">recent wastewater data\u003c/a> from Palo Alto, Sunnyvale and Davis suggest BA.2 is starting to push cases up around Northern California — the first real sign that it’s having an impact in the region.\u003c/p>\n\u003cp>But the data does not suggest a repeat of last winter’s surge.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“It’s not that sharp, dramatic increase from the beginning of the omicron wave,” said Marlene Wolfe of Emory University, one of the researchers who monitors wastewater sites across Northern California. “It’s something to watch, something to be careful of, something that we are glad we have this data to speak to.”\u003c/p>\n\u003ch2>Here’s what you need to know about BA.2 across California\u003c/h2>\n\u003cp>BA.2 is really good at its job: To date, it’s the most transmissible strain of the coronavirus. A \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.01.28.22270044v1\" target=\"_blank\" rel=\"noopener noreferrer\">Danish study\u003c/a> shows the virus spreads very quickly inside households, and a recent \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.03.26.22272984v1\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s2\">Swedish study\u003c/span>\u003c/a> shows that the viral loads are twice as high as the original omicron, which helps to explain why the latest strain of COVID-19 is furiously outcompeting its predecessor.\u003c/p>\n\u003cp>The good news is BA.2 does not appear to lead to more severe symptoms than the original omicron. Patients complain of cough, fatigue, congestion, dizziness and a runny nose.\u003c/p>\n\u003cp>“It’s not causing more intensive care hospital admissions in Europe,” said Dr. Susan Philip, San Francisco’s health officer. “[This is] a positive thing when we look at the characteristics of this virus.”\u003c/p>\n\u003ch2>How worried should we be?\u003c/h2>\n\u003cp>Not too worried, according to Dr. Bob Wachter, chair of UCSF’s department of medicine. “It might well lead to a small increase in cases, which we should watch carefully,” he said in an email. “It is unlikely to cause a major surge given the extent of [local] vax and infection-related immunity.”\u003c/p>\n\u003cp>That sentiment is shared by other local experts. UCSF epidemiologist Dr. George Rutherford suspects the impact in Northern California will be “relatively minor.” He estimates immunity coverage in the Bay Area is hovering around 90% due to high vaccine rates and the recent omicron wave, which left many people with natural immunity, at least in the short term. Those two factors wrap the region in a protective layer.\u003c/p>\n\u003cp>Rutherford points to what he sees as hopeful signs unfolding overseas. “Look at Western European data,” he said. “Cases are going up in some countries and not in others. A surge is not inevitable.”\u003c/p>\n\u003ch2>California cases continue to plummet\u003c/h2>\n\u003cp>It’s not time to panic. \u003ca href=\"https://covid19.ca.gov/?gclid=Cj0KCQjw3IqSBhCoARIsAMBkTb0HWWvfRHDNjPLxgEaX7PUdfx_IgCF7LJ77g3o8FIZ0HxBPJmRdTDIaAtYAEALw_wcB\">Cases across the state\u003c/a> have fallen about 32% over the past two weeks. Hospitalizations are not increasing and death rates continue to fall. Some regions are experiencing very slight upticks, but nothing concerning to public health officials.\u003c/p>\n\u003cp>Still, BA.2 poses the highest risk to anyone who is not vaccinated and did not catch omicron during the last surge. “The consequences for hospitalizations and deaths will be largely determined by how many people are vaccinated and how many older people are boosted,” said Bill Hanage, a Harvard epidemiologist.\u003c/p>\n\u003cp>This means children who are not yet old enough for a vaccine, as well as many disabled and immunocompromised people, remain at high risk.\u003c/p>\n\u003cp>If an actual surge were to form, regions with low vaccination rates would be the most vulnerable. In California that means rural areas and parts of the Central Valley.\u003c/p>\n\u003ch2>How can I protect myself?\u003c/h2>\n\u003cp>At this point California health officials are not recommending people make any course corrections to their daily lives. The state has a \u003ca href=\"https://files.covid19.ca.gov/pdf/smarter-plan--en.pdf\">road map for potential surges\u003c/a>, if the situation were to change.\u003c/p>\n\u003cp>“If we do start to see concerning increases in cases, increased severity or increasing hospitalization — we may need to reinstate some of our prior tools, things like masking,” California State Epidemiologist Dr. Erica Pan told KQED.\u003c/p>\n\u003cp>She recommends making sure you’re up to date on your vaccinations, and stocking up on \u003ca href=\"https://www.kqed.org/news/11901928/you-can-now-order-free-covid-at-home-tests-via-usps\"> home testing kits\u003c/a> to protect loved ones.\u003c/p>\n\u003ch2>Should I get a 4th dose if I’m over age 50?\u003c/h2>\n\u003cp>The U.S. Food and Drug Administration announced Tuesday that it has approved a fourth shot for people over 50. Until now the only people authorized for a fourth dose were those \u003ca href=\"https://www.nytimes.com/2022/01/09/health/immunocompromised-fourth-dose-booster.html\">with weakened immune systems\u003c/a>.\u003c/p>\n\u003cp>UCSF’s Wachter recommends a fourth shot for older adults who didn’t catch omicron in the last wave. This is especially critical if folks are engaging in riskier behaviors like eating inside restaurants. For those who caught the virus recently, Wachter suggests holding off on a fourth shot for a few months because a recent infection offers similar protection.\u003c/p>\n\u003cp>There’s \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.02.01.22270232v1.full.pdfre-pharmaceuticals/israeli-study-2nd-vaccine-booster-significantly-lowers-covid-death-rate-2022-03-27/\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s2\">compelling mortality data out of Israel\u003c/span>\u003c/a> suggesting a fourth shot dramatically lowers severe illness. However, the available data is preliminary and it’s not clear how long the benefits of a fourth dose will last.\u003c/p>\n\u003cp>https://twitter.com/Bob_Wachter/status/1508444987783929858?s=20&t=yr0py0rn9KRqRoEXy1Nb6Q\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“I’m going to get it when I can,” \u003ca href=\"https://twitter.com/Bob_Wachter/status/1508446942887485440?s=20&t=yr0py0rn9KRqRoEXy1Nb6Q\">Wachter said in another tweet\u003c/a>. “I see the advantages of the 2nd boost as outweighing the small potential downside.”\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>We’ve seen this play out before: Just as we start letting down our guard, the coronavirus mutates into another insidious version, wreaking havoc on our plans.\u003c/p>\n\u003cp>Cue BA.2, or \u003ca href=\"https://www.ama-assn.org/delivering-care/public-health/what-ba2-or-stealth-omicron-subvariant\">stealth omicron\u003c/a>.\u003c/p>\n\u003cp>Earlier this month when mask mandates started falling away, the subvariant struck parts of Europe and Asia, driving \u003ca href=\"https://www.cnbc.com/2022/03/23/omicrons-subvariant-bapoint2-could-spread-wildly-in-europe-epidemiologist.html\">unprecedented spikes\u003c/a>. Now, it’s traveling fast within the U.S.\u003c/p>\n\u003cp>BA.2 is both the dominant strain globally and, now, nationally, according to the \u003ca href=\"https://covid.cdc.gov/covid-data-tracker/#variant-proportions\" target=\"_blank\" rel=\"noopener noreferrer\">Centers for Disease Control and Prevention\u003c/a>, which credits more than half of U.S. cases to stealth omicron. Infections are edging up in parts of the Northeast, and \u003ca href=\"https://soe-wbe-pilot.wl.r.appspot.com/charts#page=overview\">recent wastewater data\u003c/a> from Palo Alto, Sunnyvale and Davis suggest BA.2 is starting to push cases up around Northern California — the first real sign that it’s having an impact in the region.\u003c/p>\n\u003cp>But the data does not suggest a repeat of last winter’s surge.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“It’s not that sharp, dramatic increase from the beginning of the omicron wave,” said Marlene Wolfe of Emory University, one of the researchers who monitors wastewater sites across Northern California. “It’s something to watch, something to be careful of, something that we are glad we have this data to speak to.”\u003c/p>\n\u003ch2>Here’s what you need to know about BA.2 across California\u003c/h2>\n\u003cp>BA.2 is really good at its job: To date, it’s the most transmissible strain of the coronavirus. A \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.01.28.22270044v1\" target=\"_blank\" rel=\"noopener noreferrer\">Danish study\u003c/a> shows the virus spreads very quickly inside households, and a recent \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.03.26.22272984v1\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s2\">Swedish study\u003c/span>\u003c/a> shows that the viral loads are twice as high as the original omicron, which helps to explain why the latest strain of COVID-19 is furiously outcompeting its predecessor.\u003c/p>\n\u003cp>The good news is BA.2 does not appear to lead to more severe symptoms than the original omicron. Patients complain of cough, fatigue, congestion, dizziness and a runny nose.\u003c/p>\n\u003cp>“It’s not causing more intensive care hospital admissions in Europe,” said Dr. Susan Philip, San Francisco’s health officer. “[This is] a positive thing when we look at the characteristics of this virus.”\u003c/p>\n\u003ch2>How worried should we be?\u003c/h2>\n\u003cp>Not too worried, according to Dr. Bob Wachter, chair of UCSF’s department of medicine. “It might well lead to a small increase in cases, which we should watch carefully,” he said in an email. “It is unlikely to cause a major surge given the extent of [local] vax and infection-related immunity.”\u003c/p>\n\u003cp>That sentiment is shared by other local experts. UCSF epidemiologist Dr. George Rutherford suspects the impact in Northern California will be “relatively minor.” He estimates immunity coverage in the Bay Area is hovering around 90% due to high vaccine rates and the recent omicron wave, which left many people with natural immunity, at least in the short term. Those two factors wrap the region in a protective layer.\u003c/p>\n\u003cp>Rutherford points to what he sees as hopeful signs unfolding overseas. “Look at Western European data,” he said. “Cases are going up in some countries and not in others. A surge is not inevitable.”\u003c/p>\n\u003ch2>California cases continue to plummet\u003c/h2>\n\u003cp>It’s not time to panic. \u003ca href=\"https://covid19.ca.gov/?gclid=Cj0KCQjw3IqSBhCoARIsAMBkTb0HWWvfRHDNjPLxgEaX7PUdfx_IgCF7LJ77g3o8FIZ0HxBPJmRdTDIaAtYAEALw_wcB\">Cases across the state\u003c/a> have fallen about 32% over the past two weeks. Hospitalizations are not increasing and death rates continue to fall. Some regions are experiencing very slight upticks, but nothing concerning to public health officials.\u003c/p>\n\u003cp>Still, BA.2 poses the highest risk to anyone who is not vaccinated and did not catch omicron during the last surge. “The consequences for hospitalizations and deaths will be largely determined by how many people are vaccinated and how many older people are boosted,” said Bill Hanage, a Harvard epidemiologist.\u003c/p>\n\u003cp>This means children who are not yet old enough for a vaccine, as well as many disabled and immunocompromised people, remain at high risk.\u003c/p>\n\u003cp>If an actual surge were to form, regions with low vaccination rates would be the most vulnerable. In California that means rural areas and parts of the Central Valley.\u003c/p>\n\u003ch2>How can I protect myself?\u003c/h2>\n\u003cp>At this point California health officials are not recommending people make any course corrections to their daily lives. The state has a \u003ca href=\"https://files.covid19.ca.gov/pdf/smarter-plan--en.pdf\">road map for potential surges\u003c/a>, if the situation were to change.\u003c/p>\n\u003cp>“If we do start to see concerning increases in cases, increased severity or increasing hospitalization — we may need to reinstate some of our prior tools, things like masking,” California State Epidemiologist Dr. Erica Pan told KQED.\u003c/p>\n\u003cp>She recommends making sure you’re up to date on your vaccinations, and stocking up on \u003ca href=\"https://www.kqed.org/news/11901928/you-can-now-order-free-covid-at-home-tests-via-usps\"> home testing kits\u003c/a> to protect loved ones.\u003c/p>\n\u003ch2>Should I get a 4th dose if I’m over age 50?\u003c/h2>\n\u003cp>The U.S. Food and Drug Administration announced Tuesday that it has approved a fourth shot for people over 50. Until now the only people authorized for a fourth dose were those \u003ca href=\"https://www.nytimes.com/2022/01/09/health/immunocompromised-fourth-dose-booster.html\">with weakened immune systems\u003c/a>.\u003c/p>\n\u003cp>UCSF’s Wachter recommends a fourth shot for older adults who didn’t catch omicron in the last wave. This is especially critical if folks are engaging in riskier behaviors like eating inside restaurants. For those who caught the virus recently, Wachter suggests holding off on a fourth shot for a few months because a recent infection offers similar protection.\u003c/p>\n\u003cp>There’s \u003ca href=\"https://www.medrxiv.org/content/10.1101/2022.02.01.22270232v1.full.pdfre-pharmaceuticals/israeli-study-2nd-vaccine-booster-significantly-lowers-covid-death-rate-2022-03-27/\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s2\">compelling mortality data out of Israel\u003c/span>\u003c/a> suggesting a fourth shot dramatically lowers severe illness. However, the available data is preliminary and it’s not clear how long the benefits of a fourth dose will last.\u003c/p>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\n\u003cp>\u003c/p>\n\u003cp>“I’m going to get it when I can,” \u003ca href=\"https://twitter.com/Bob_Wachter/status/1508446942887485440?s=20&t=yr0py0rn9KRqRoEXy1Nb6Q\">Wachter said in another tweet\u003c/a>. “I see the advantages of the 2nd boost as outweighing the small potential downside.”\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "Omicron Was in California Before It Was Named Omicron, According to Sewage Samples",
"headTitle": "Omicron Was in California Before It Was Named Omicron, According to Sewage Samples | KQED",
"content": "\u003cp>We’ve learned a lot about COVID-19 by examining what we’ve flushed down the toilet.\u003c/p>\n\u003cp>Here are a few of those things.\u003c/p>\n\u003cp>The variant was in a waste sample collected in Merced County on Nov. 25 — that’s a day before the World Health Organization named it omicron.\u003c/p>\n\u003cp>Scientists in New York found it in a sample collected even earlier, on Nov. 21, predating the alarms from leaders in South Africa about a troubling new variant.\u003c/p>\n\u003cp>Officials in Texas also detected omicron early through wastewater surveillance.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>A new \u003ca href=\"https://www.cdc.gov/mmwr/volumes/71/wr/mm7103a5.htm?s_cid=mm7103a5_w&utm_source=STAT+Newsletters&utm_campaign=6439030dc2-MR_COPY_01&utm_medium=email&utm_term=0_8cab1d7961-6439030dc2-151495997#T1_down\">\u003cspan class=\"s1\">report\u003c/span>\u003c/a> last week from the Centers for Disease Control and Prevention outlined these facts.\u003c/p>\n\u003cp>Agency scientists describe this as “strong early evidence that the Omicron variant was likely present or more widely distributed in these communities than originally indicated by clinical testing alone.”\u003c/p>\n\u003cp>The report makes a case that by the time officials have detected a new variant, it likely has spread to numerous other countries.\u003c/p>\n\u003cp>In this light, travel bans look ineffective and like “closing the barn door after the horses have fled,” as researchers from the University of Illinois argued in a \u003ca href=\"https://thehill.com/opinion/healthcare/583337-omicron-is-already-global-tests-for-international-flights-are-far-better\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">recent op-ed\u003c/span>\u003c/a>.\u003c/p>\n\u003cp>Requiring testing on international flights would be a much more effective policy, they wrote.\u003c/p>\n\u003cp>The study also underscores the potency of this new surveillance tool, which counties increasingly rely on as demand for COVID-19 tests outpace supply.\u003c/p>\n\u003cp>“The ability to ramp up the infrastructure to test the number of people that need to be tested right now is an enormous strain on the health care system and on our testing systems that we’ve set up,” said Marlene Wolfe of Emory University, one of the researchers who monitors sites across Northern California. “But with this wastewater data, we have not had to increase our capacity at all. We are doing exactly what we’ve been doing for a year.”\u003c/p>\n\u003cp>Wolfe’s method can detect as few as one or two cases per 100,000 people.\u003c/p>\n\u003cp>“We’re in close communication with public health officials,” she said. “They’re able to use that data to plan for what’s next. It’s similar to how they would use clinical case data but is actually more reliable. We are not biased by the fact that it’s so difficult to find a test right now.”\u003c/p>\n\u003cp>Wolfe says this moment is a good opportunity to expand the surveillance regime and collect data on other diseases.\u003c/p>\n\u003cp>“We’re starting to monitor for \u003ca href=\"https://www.cdc.gov/rsv/index.html\" target=\"_blank\" rel=\"noopener noreferrer\">respiratory syncytial virus\u003c/a> and influenza,” she said. “There are a lot of areas where we can provide very useful public health data using wastewater because we have developed these tools so fully over the course of this pandemic.”\u003c/p>\n\u003cp>Not all of the information in the CDC’s report is new, although now it’s been verified by federal scientists.\u003c/p>\n\u003cp>KQED’s Raquel Maria Dillon was the first to \u003ca href=\"https://www.kqed.org/news/11898161/scientists-find-traces-of-omicron-in-sewage-from-sacramento-and-merced\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">report\u003c/span>\u003c/a> on the detection in Merced, as well as a similar sample found in Sacramento on Nov. 30 — that’s a day before health officials confirmed the \u003ca href=\"https://www.kqed.org/science/1977807/first-u-s-case-of-omicron-variant-found-in-california\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">first U.S. case in a San Francisco resident on Dec. 1\u003c/span>\u003c/a>.\u003cspan class=\"Apple-converted-space\"> \u003c/span>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Researchers notified Sacramento of the findings, and officials there described the data as useful and “one of the tools that helps us identify new variants.”\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>A new \u003ca href=\"https://www.cdc.gov/mmwr/volumes/71/wr/mm7103a5.htm?s_cid=mm7103a5_w&utm_source=STAT+Newsletters&utm_campaign=6439030dc2-MR_COPY_01&utm_medium=email&utm_term=0_8cab1d7961-6439030dc2-151495997#T1_down\">\u003cspan class=\"s1\">report\u003c/span>\u003c/a> last week from the Centers for Disease Control and Prevention outlined these facts.\u003c/p>\n\u003cp>Agency scientists describe this as “strong early evidence that the Omicron variant was likely present or more widely distributed in these communities than originally indicated by clinical testing alone.”\u003c/p>\n\u003cp>The report makes a case that by the time officials have detected a new variant, it likely has spread to numerous other countries.\u003c/p>\n\u003cp>In this light, travel bans look ineffective and like “closing the barn door after the horses have fled,” as researchers from the University of Illinois argued in a \u003ca href=\"https://thehill.com/opinion/healthcare/583337-omicron-is-already-global-tests-for-international-flights-are-far-better\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">recent op-ed\u003c/span>\u003c/a>.\u003c/p>\n\u003cp>Requiring testing on international flights would be a much more effective policy, they wrote.\u003c/p>\n\u003cp>The study also underscores the potency of this new surveillance tool, which counties increasingly rely on as demand for COVID-19 tests outpace supply.\u003c/p>\n\u003cp>“The ability to ramp up the infrastructure to test the number of people that need to be tested right now is an enormous strain on the health care system and on our testing systems that we’ve set up,” said Marlene Wolfe of Emory University, one of the researchers who monitors sites across Northern California. “But with this wastewater data, we have not had to increase our capacity at all. We are doing exactly what we’ve been doing for a year.”\u003c/p>\n\u003cp>Wolfe’s method can detect as few as one or two cases per 100,000 people.\u003c/p>\n\u003cp>“We’re in close communication with public health officials,” she said. “They’re able to use that data to plan for what’s next. It’s similar to how they would use clinical case data but is actually more reliable. We are not biased by the fact that it’s so difficult to find a test right now.”\u003c/p>\n\u003cp>Wolfe says this moment is a good opportunity to expand the surveillance regime and collect data on other diseases.\u003c/p>\n\u003cp>“We’re starting to monitor for \u003ca href=\"https://www.cdc.gov/rsv/index.html\" target=\"_blank\" rel=\"noopener noreferrer\">respiratory syncytial virus\u003c/a> and influenza,” she said. “There are a lot of areas where we can provide very useful public health data using wastewater because we have developed these tools so fully over the course of this pandemic.”\u003c/p>\n\u003cp>Not all of the information in the CDC’s report is new, although now it’s been verified by federal scientists.\u003c/p>\n\u003cp>KQED’s Raquel Maria Dillon was the first to \u003ca href=\"https://www.kqed.org/news/11898161/scientists-find-traces-of-omicron-in-sewage-from-sacramento-and-merced\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">report\u003c/span>\u003c/a> on the detection in Merced, as well as a similar sample found in Sacramento on Nov. 30 — that’s a day before health officials confirmed the \u003ca href=\"https://www.kqed.org/science/1977807/first-u-s-case-of-omicron-variant-found-in-california\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cspan class=\"s1\">first U.S. case in a San Francisco resident on Dec. 1\u003c/span>\u003c/a>.\u003cspan class=\"Apple-converted-space\"> \u003c/span>\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>Researchers notified Sacramento of the findings, and officials there described the data as useful and “one of the tools that helps us identify new variants.”\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "Here Are 8 Lingering Questions About the New COVID Pills From Merck and Pfizer",
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"content": "\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">T\u003c/span>\u003c/span>he past two months have brought extremely good news in the fight against COVID-19. Two different oral treatments have proved effective at both preventing people newly diagnosed with COVID-19 from entering the hospital and from dying.\u003c/p>\n\u003cp>“We’re accelerating our path out of this pandemic,” President Biden said after data on the second COVID pill became available. The wide availability of oral drugs could make COVID-19 less lethal, making it less risky for people to return to in-person work and to their normal lives.\u003c/p>\n\u003cp>The \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">first results\u003c/a>, from Merck and Ridgeback Therapeutics, were released in October and will be considered by an advisory panel to the Food and Drug Administration in December. That could lead to an emergency use authorization in the U.S. by the end of the year. That drug, molnupiravir, reduced hospitalizations by 50% and prevented deaths entirely a large randomized clinical trial when it was given within five days of when symptoms began. The pill is given as a five-day course during which patients take a total of 40 pills.\u003c/p>\n\u003cp>In November, Pfizer announced that its COVID pill, Paxlovid, reduced hospitalizations by 89% and also prevented deaths in its own large randomized study. As with the Merck drug, Paxlovid is given as a five-day course. It must be given with a second medicine, a booster, called ritonavir, which is made by AbbVie, another large drug firm. The Pfizer regimen involves taking 30 pills over a five-day period.\u003c/p>\n\u003cp>Though the topline results are similar, the medicines could have different risks and benefits. The companies have only issued data in press releases, not scientific articles, and doctors need to know a lot more about both. Here is an overview of what we still don’t know about the COVID pills and when we might learn it.\u003c/p>\n\u003ch3>Which one works better?\u003c/h3>\n\u003cp>At the headline level, Pfizer’s pill reduced the risk of hospitalization and death \u003ca href=\"https://www.statnews.com/2021/11/05/experimental-pfizer-pill-prevents-covid-hospitalizations-and-deaths/\" target=\"_blank\" rel=\"noopener noreferrer\">by 89%,\u003c/a> while Merck showed \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">a reduction of 50%\u003c/a>. But neither firm has disclosed detailed data from its pivotal studies, and the trials were not identically designed.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The studies enrolled similar populations — unvaccinated people with mild to moderate COVID-19 and at least one risk factor for severe disease — but they had slightly different measures of efficacy. Pfizer’s 89% figure comes from patients who started getting its pill, Paxlovid, within three days of their first COVID-19 symptoms. Merck’s 50% applies to patients who began treatment within five days. In the Paxlovid study, patients who started treatment within five days saw an 85% improvement in hospitalization or death versus placebo. Merck has not shared data on patients who got its drug within three days of symptom onset.\u003c/p>\n\u003cp>What the studies had in common was 100% efficacy against death, regardless of when patients started treatment. Merck’s study counted eight deaths among patients on placebo, and Pfizer’s observed 10.\u003c/p>\n\u003cp>On the safety side, the rate of side effects in both studies was similar between the treatment groups and placebo groups. In each study, fewer patients in the treatment group left the study due to side effects compared to those in the placebo group. Neither company has disclosed detailed data on the type and severity of side effects.\u003c/p>\n\u003cp>Each treatment is administered twice a day for five total days, amounting to 10 doses in total. Pfizer’s drug is co-administered with a common antiviral called ritonavir.\u003c/p>\n\u003ch3>Will the antiviral be available for vaccinated patients with breakthrough infections?\u003c/h3>\n\u003cp>Both companies conducted their studies entirely in patients who were at high risk of complications if they caught COVID and who also had not been vaccinated. That leads to a big question for policymakers: Should those who have been vaccinated, but who develop a breakthrough infection of SARS-CoV-2, be given the pills?\u003c/p>\n\u003cp>Right now that is a question without data. A third antiviral pill, from the biotech firm Atea and the large drug firm Roche, failed to prove it was effective in its own study, and Wall Street analysts suspect the reason is that the companies included vaccinated patients in the research. For those who have received the vaccine, hospitalization and death are much less likely. This means that it is harder for a drug to show efficacy, because there are fewer infections to prevent.\u003c/p>\n\u003cp>So regulators and public health officials will have to make a judgement on the risks and benefits of the COVID pills for people with breakthrough infections — without direct data in these populations.\u003c/p>\n\u003cp>Pfizer is running a clinical trial, with results due next year, that does include vaccinated patients, and the company’s executives have expressed confidence based on the results so far that the treatment should work. Both Merck and Pfizer are also running studies to show that the drugs can prevent people from developing symptoms if they take the antivirals after they are exposed to the virus.\u003c/p>\n\u003ch3>Do the drugs work the same way?\u003c/h3>\n\u003cp>No, not really. While both drugs interfere with the process the coronavirus uses to reproduce itself, each drug interferes at a very different point.\u003c/p>\n\u003cp>Merck’s drug throws a wrench into the works quite early. After someone takes molnupiravir, the drug is transformed into something uncannily similar to one of RNA’s chemical building blocks.\u003c/p>\n\u003cp>The modification is so subtle that not only will the coronavirus use molnupiravir in place of other building blocks when it replicates itself, but coronaviruses’ unusual proofreading mechanism can’t even pick up on the imposter compound. Over time, the drug will encourage the virus to introduce even more mistakes.\u003c/p>\n\u003cp>“Ultimately, this leads to what’s known as error catastrophe. It’s introducing so many different mutations that, eventually, nothing further can happen,” said Katherine Seley-Radtke, a medicinal chemist at the University of Maryland, Baltimore County. “You’ve got this completely mutated RNA.”\u003c/p>\n\u003cp>Pfizer’s drug, Paxlovid, acts at a completely different point in the virus’ reproductive process.\u003c/p>\n\u003cp>“It’s apples and oranges,” said Ronald Swanstrom, a biochemistry professor at the University of North Carolina School of Medicine.\u003c/p>\n\u003cp>Unlike molnupiravir, Paxlovid allows the strings of viral RNA to be assembled correctly. It even allows those strings to be used to create viral proteins, which are initially produced in one big chunk. Like a bolt of fabric before it’s cut to a clothing pattern, this protein needs to be chopped down to size before it can work.\u003c/p>\n\u003cp>That cutting is what Paxlovid prohibits. The drug is designed to bind to a particularly important point in an enzyme called a protease which slices up proteins. Without a functioning protease, the virus can’t create functional copies; no working virus, no problem.\u003c/p>\n\u003cp>Protease inhibitors have been used for decades to create more than a dozen drugs for HIV and hepatitis C; in some cases, they’ve also been used as cancer drugs.\u003c/p>\n\u003cp>“There’s a long history of medicinal chemistry targeting proteases,” said Bryan Dickinson, a chemical biologist at the University of Chicago.\u003c/p>\n\u003cp>Paxlovid is designed with a SARS-CoV-2-specific protease in mind, so it works more specifically on this coronavirus than molnupiravir.\u003c/p>\n\u003cp>But Paxlovid can’t work as well if it’s taken on its own. The body’s defense mechanisms will get rid of anything that it doesn’t recognize — including drugs, which can be digested by enzymes in a person’s liver. Another drug called ritonavir blocks the liver enzyme that would likely chew up Paxlovid, which gives the latter drug the space it needs to work.\u003c/p>\n\u003ch3>How do they compare with monoclonal antibodies?\u003c/h3>\n\u003cp>Regeneron Pharmaceuticals and Eli Lilly have each won FDA authorization for antibody combination therapies that keep recently diagnosed COVID-19 patients from hospitalization and death. In a Phase 3 study enrolling recently diagnosed patients at high risk for severe disease, Regeneron’s treatment reduced the risk of hospitalization or death \u003ca href=\"https://investor.regeneron.com/news-releases/news-release-details/phase-3-trial-shows-regen-covtm-casirivimab-imdevimab-antibody\" target=\"_blank\" rel=\"noopener noreferrer\">by 70%\u003c/a> compared to placebo. In a similar study, Lilly’s therapy showed \u003ca href=\"https://www.prnewswire.com/news-releases/lillys-bamlanivimab-and-etesevimab-together-reduced-hospitalizations-and-death-in-phase-3-trial-for-early-covid-19-301243984.html\" target=\"_blank\" rel=\"noopener noreferrer\">an 87% reduction\u003c/a>.\u003c/p>\n\u003cp>The biggest difference is one of convenience. The antibody treatments are administered intravenously in a one-time, roughly hour-long process (Regeneron’s is authorized for subcutaneous injection when an IV procedure is not feasible). That could make the treatments from Pfizer and Merck, taken orally at home, preferable to patients unable to visit an infusion center.\u003c/p>\n\u003cp>There’s also a difference in cost. Regeneron and Lilly have signed deals with the federal government to sell their treatments at about $1,250 per dose. Merck’s agreement with the U.S. works out to about $700 for a five-day course of molnupiravir. Pfizer is still negotiating contracts but is expected to set a similar price for Paxlovid.\u003c/p>\n\u003ch3>How easy will they be to get?\u003c/h3>\n\u003cp>A pill is a huge leap in terms of logistical ease over infused therapies like monoclonal antibodies. For those treatments, not only did people have to make their way to clinics for their infusions, but hospitals and other facilities had to set up places where people who were actively infectious could come get treated without risking others’ health. (The other antiviral authorized to treat COVID-19, Gilead’s remdesivir, is an infusion and approved only for hospitalized patients, but some data indicate that if it were to be given to patients earlier in their infections, it could have a greater effect. If its approval ever covered outpatients, however, it would still run into the same logistical challenges of an infused therapy.)\u003c/p>\n\u003cp>Still, the COVID pills come with a key challenge of their own. They’re most effective when given early in the infection, so people need to be able to get tested and get their prescription rapidly. And the U.S. testing landscape is still limited. PCR tests can take days to return a result, and though the Biden administration has upped its effort to expand the availability of at-home rapid tests, finding one at a store is still hit or miss — success feels like scoring this holiday season’s hottest gift. Any delay in getting diagnosed undercuts the power of these pills; even a day or two has real implications for a treatment meant to clear out an acute infection like COVID-19.\u003c/p>\n\u003ch3>Will it affect a patient’s DNA?\u003c/h3>\n\u003cp>This is really a question only for Merck’s molnupiravir, since it works by sneaking subtly corrupted parts into the coronavirus’s RNA sequence.\u003c/p>\n\u003cp>Once the virus has mutated too much, it can’t work — mission accomplished. But there’s a theoretical chance that molnupiravir could also influence normal human DNA when it replicates, too. If mutations happen during that process, it could spell real trouble.\u003c/p>\n\u003cp>Merck did some tests during molnupiravir’s development to check this possibility out. In two different types of animal studies using higher and longer doses than are given to humans, Merck’s scientists didn’t see any increased risk of unwanted mutations.\u003c/p>\n\u003cp>“We are very confident in the safety profile of molnupiravir based on our preclinical and clinical data,” executive vice president Dean Li told investors in an October conference call, according to a transcript in the financial database Sentieo.\u003c/p>\n\u003cp>But UNC’s Swanstrom isn’t completely convinced that the tests Merck did were sensitive enough. In August, he and his colleagues \u003ca href=\"https://pubmed.ncbi.nlm.nih.gov/33961695/\" target=\"_blank\" rel=\"noopener noreferrer\">published a paper in\u003c/a> the Journal of Infectious Diseases showing that a key metabolite of molnupiravir could mutate DNA in animal cells.\u003c/p>\n\u003cp>Given these results, Swanstrom said he would be particularly interested in seeing a long-term study of people who took molnupiravir to continue to monitor this potential effect over the next 10 or 20 years.\u003c/p>\n\u003cp>“This thing is going to go into thousands of people. And are we just going to ignore the fact that there’s this potential risk?” he said. “The risk could be zero. It could be no worse than going to get a dental X-ray — or it could do something more. But unless we find out, you know, we’re going to learn this lesson the hard way, way later than we should.”\u003c/p>\n\u003ch3>What might the new antivirals mean for cancer patients?\u003c/h3>\n\u003cp>Because the new antiviral Pfizer is developing is a protease inhibitor, infectious disease specialists are familiar with how it works. So we already know: These drugs have the potential to interfere with many therapies used to treat cancer, Tobias Hohl, chief of the infectious diseases service at Memorial Sloan Kettering Cancer Center in New York, told STAT.\u003c/p>\n\u003cp>“They’re going to be very helpful [in our] armamentarium, but they will not substitute for prevention or vaccination efforts because these are not medicines that are completely benign and harmless in terms of their drug-drug interactions and toxicity,” he said. “So we’re going to have to be careful and thoughtful about how we use our protease inhibitors.”\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>Matthew Herper, Damian Garde, Kate Sheridan, Adam Feuerstein, Andrew Joseph, and Elizabeth Cooney contributed reporting.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">T\u003c/span>\u003c/span>he past two months have brought extremely good news in the fight against COVID-19. Two different oral treatments have proved effective at both preventing people newly diagnosed with COVID-19 from entering the hospital and from dying.\u003c/p>\n\u003cp>“We’re accelerating our path out of this pandemic,” President Biden said after data on the second COVID pill became available. The wide availability of oral drugs could make COVID-19 less lethal, making it less risky for people to return to in-person work and to their normal lives.\u003c/p>\n\u003cp>The \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">first results\u003c/a>, from Merck and Ridgeback Therapeutics, were released in October and will be considered by an advisory panel to the Food and Drug Administration in December. That could lead to an emergency use authorization in the U.S. by the end of the year. That drug, molnupiravir, reduced hospitalizations by 50% and prevented deaths entirely a large randomized clinical trial when it was given within five days of when symptoms began. The pill is given as a five-day course during which patients take a total of 40 pills.\u003c/p>\n\u003cp>In November, Pfizer announced that its COVID pill, Paxlovid, reduced hospitalizations by 89% and also prevented deaths in its own large randomized study. As with the Merck drug, Paxlovid is given as a five-day course. It must be given with a second medicine, a booster, called ritonavir, which is made by AbbVie, another large drug firm. The Pfizer regimen involves taking 30 pills over a five-day period.\u003c/p>\n\u003cp>Though the topline results are similar, the medicines could have different risks and benefits. The companies have only issued data in press releases, not scientific articles, and doctors need to know a lot more about both. Here is an overview of what we still don’t know about the COVID pills and when we might learn it.\u003c/p>\n\u003ch3>Which one works better?\u003c/h3>\n\u003cp>At the headline level, Pfizer’s pill reduced the risk of hospitalization and death \u003ca href=\"https://www.statnews.com/2021/11/05/experimental-pfizer-pill-prevents-covid-hospitalizations-and-deaths/\" target=\"_blank\" rel=\"noopener noreferrer\">by 89%,\u003c/a> while Merck showed \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">a reduction of 50%\u003c/a>. But neither firm has disclosed detailed data from its pivotal studies, and the trials were not identically designed.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The studies enrolled similar populations — unvaccinated people with mild to moderate COVID-19 and at least one risk factor for severe disease — but they had slightly different measures of efficacy. Pfizer’s 89% figure comes from patients who started getting its pill, Paxlovid, within three days of their first COVID-19 symptoms. Merck’s 50% applies to patients who began treatment within five days. In the Paxlovid study, patients who started treatment within five days saw an 85% improvement in hospitalization or death versus placebo. Merck has not shared data on patients who got its drug within three days of symptom onset.\u003c/p>\n\u003cp>What the studies had in common was 100% efficacy against death, regardless of when patients started treatment. Merck’s study counted eight deaths among patients on placebo, and Pfizer’s observed 10.\u003c/p>\n\u003cp>On the safety side, the rate of side effects in both studies was similar between the treatment groups and placebo groups. In each study, fewer patients in the treatment group left the study due to side effects compared to those in the placebo group. Neither company has disclosed detailed data on the type and severity of side effects.\u003c/p>\n\u003cp>Each treatment is administered twice a day for five total days, amounting to 10 doses in total. Pfizer’s drug is co-administered with a common antiviral called ritonavir.\u003c/p>\n\u003ch3>Will the antiviral be available for vaccinated patients with breakthrough infections?\u003c/h3>\n\u003cp>Both companies conducted their studies entirely in patients who were at high risk of complications if they caught COVID and who also had not been vaccinated. That leads to a big question for policymakers: Should those who have been vaccinated, but who develop a breakthrough infection of SARS-CoV-2, be given the pills?\u003c/p>\n\u003cp>Right now that is a question without data. A third antiviral pill, from the biotech firm Atea and the large drug firm Roche, failed to prove it was effective in its own study, and Wall Street analysts suspect the reason is that the companies included vaccinated patients in the research. For those who have received the vaccine, hospitalization and death are much less likely. This means that it is harder for a drug to show efficacy, because there are fewer infections to prevent.\u003c/p>\n\u003cp>So regulators and public health officials will have to make a judgement on the risks and benefits of the COVID pills for people with breakthrough infections — without direct data in these populations.\u003c/p>\n\u003cp>Pfizer is running a clinical trial, with results due next year, that does include vaccinated patients, and the company’s executives have expressed confidence based on the results so far that the treatment should work. Both Merck and Pfizer are also running studies to show that the drugs can prevent people from developing symptoms if they take the antivirals after they are exposed to the virus.\u003c/p>\n\u003ch3>Do the drugs work the same way?\u003c/h3>\n\u003cp>No, not really. While both drugs interfere with the process the coronavirus uses to reproduce itself, each drug interferes at a very different point.\u003c/p>\n\u003cp>Merck’s drug throws a wrench into the works quite early. After someone takes molnupiravir, the drug is transformed into something uncannily similar to one of RNA’s chemical building blocks.\u003c/p>\n\u003cp>The modification is so subtle that not only will the coronavirus use molnupiravir in place of other building blocks when it replicates itself, but coronaviruses’ unusual proofreading mechanism can’t even pick up on the imposter compound. Over time, the drug will encourage the virus to introduce even more mistakes.\u003c/p>\n\u003cp>“Ultimately, this leads to what’s known as error catastrophe. It’s introducing so many different mutations that, eventually, nothing further can happen,” said Katherine Seley-Radtke, a medicinal chemist at the University of Maryland, Baltimore County. “You’ve got this completely mutated RNA.”\u003c/p>\n\u003cp>Pfizer’s drug, Paxlovid, acts at a completely different point in the virus’ reproductive process.\u003c/p>\n\u003cp>“It’s apples and oranges,” said Ronald Swanstrom, a biochemistry professor at the University of North Carolina School of Medicine.\u003c/p>\n\u003cp>Unlike molnupiravir, Paxlovid allows the strings of viral RNA to be assembled correctly. It even allows those strings to be used to create viral proteins, which are initially produced in one big chunk. Like a bolt of fabric before it’s cut to a clothing pattern, this protein needs to be chopped down to size before it can work.\u003c/p>\n\u003cp>That cutting is what Paxlovid prohibits. The drug is designed to bind to a particularly important point in an enzyme called a protease which slices up proteins. Without a functioning protease, the virus can’t create functional copies; no working virus, no problem.\u003c/p>\n\u003cp>Protease inhibitors have been used for decades to create more than a dozen drugs for HIV and hepatitis C; in some cases, they’ve also been used as cancer drugs.\u003c/p>\n\u003cp>“There’s a long history of medicinal chemistry targeting proteases,” said Bryan Dickinson, a chemical biologist at the University of Chicago.\u003c/p>\n\u003cp>Paxlovid is designed with a SARS-CoV-2-specific protease in mind, so it works more specifically on this coronavirus than molnupiravir.\u003c/p>\n\u003cp>But Paxlovid can’t work as well if it’s taken on its own. The body’s defense mechanisms will get rid of anything that it doesn’t recognize — including drugs, which can be digested by enzymes in a person’s liver. Another drug called ritonavir blocks the liver enzyme that would likely chew up Paxlovid, which gives the latter drug the space it needs to work.\u003c/p>\n\u003ch3>How do they compare with monoclonal antibodies?\u003c/h3>\n\u003cp>Regeneron Pharmaceuticals and Eli Lilly have each won FDA authorization for antibody combination therapies that keep recently diagnosed COVID-19 patients from hospitalization and death. In a Phase 3 study enrolling recently diagnosed patients at high risk for severe disease, Regeneron’s treatment reduced the risk of hospitalization or death \u003ca href=\"https://investor.regeneron.com/news-releases/news-release-details/phase-3-trial-shows-regen-covtm-casirivimab-imdevimab-antibody\" target=\"_blank\" rel=\"noopener noreferrer\">by 70%\u003c/a> compared to placebo. In a similar study, Lilly’s therapy showed \u003ca href=\"https://www.prnewswire.com/news-releases/lillys-bamlanivimab-and-etesevimab-together-reduced-hospitalizations-and-death-in-phase-3-trial-for-early-covid-19-301243984.html\" target=\"_blank\" rel=\"noopener noreferrer\">an 87% reduction\u003c/a>.\u003c/p>\n\u003cp>The biggest difference is one of convenience. The antibody treatments are administered intravenously in a one-time, roughly hour-long process (Regeneron’s is authorized for subcutaneous injection when an IV procedure is not feasible). That could make the treatments from Pfizer and Merck, taken orally at home, preferable to patients unable to visit an infusion center.\u003c/p>\n\u003cp>There’s also a difference in cost. Regeneron and Lilly have signed deals with the federal government to sell their treatments at about $1,250 per dose. Merck’s agreement with the U.S. works out to about $700 for a five-day course of molnupiravir. Pfizer is still negotiating contracts but is expected to set a similar price for Paxlovid.\u003c/p>\n\u003ch3>How easy will they be to get?\u003c/h3>\n\u003cp>A pill is a huge leap in terms of logistical ease over infused therapies like monoclonal antibodies. For those treatments, not only did people have to make their way to clinics for their infusions, but hospitals and other facilities had to set up places where people who were actively infectious could come get treated without risking others’ health. (The other antiviral authorized to treat COVID-19, Gilead’s remdesivir, is an infusion and approved only for hospitalized patients, but some data indicate that if it were to be given to patients earlier in their infections, it could have a greater effect. If its approval ever covered outpatients, however, it would still run into the same logistical challenges of an infused therapy.)\u003c/p>\n\u003cp>Still, the COVID pills come with a key challenge of their own. They’re most effective when given early in the infection, so people need to be able to get tested and get their prescription rapidly. And the U.S. testing landscape is still limited. PCR tests can take days to return a result, and though the Biden administration has upped its effort to expand the availability of at-home rapid tests, finding one at a store is still hit or miss — success feels like scoring this holiday season’s hottest gift. Any delay in getting diagnosed undercuts the power of these pills; even a day or two has real implications for a treatment meant to clear out an acute infection like COVID-19.\u003c/p>\n\u003ch3>Will it affect a patient’s DNA?\u003c/h3>\n\u003cp>This is really a question only for Merck’s molnupiravir, since it works by sneaking subtly corrupted parts into the coronavirus’s RNA sequence.\u003c/p>\n\u003cp>Once the virus has mutated too much, it can’t work — mission accomplished. But there’s a theoretical chance that molnupiravir could also influence normal human DNA when it replicates, too. If mutations happen during that process, it could spell real trouble.\u003c/p>\n\u003cp>Merck did some tests during molnupiravir’s development to check this possibility out. In two different types of animal studies using higher and longer doses than are given to humans, Merck’s scientists didn’t see any increased risk of unwanted mutations.\u003c/p>\n\u003cp>“We are very confident in the safety profile of molnupiravir based on our preclinical and clinical data,” executive vice president Dean Li told investors in an October conference call, according to a transcript in the financial database Sentieo.\u003c/p>\n\u003cp>But UNC’s Swanstrom isn’t completely convinced that the tests Merck did were sensitive enough. In August, he and his colleagues \u003ca href=\"https://pubmed.ncbi.nlm.nih.gov/33961695/\" target=\"_blank\" rel=\"noopener noreferrer\">published a paper in\u003c/a> the Journal of Infectious Diseases showing that a key metabolite of molnupiravir could mutate DNA in animal cells.\u003c/p>\n\u003cp>Given these results, Swanstrom said he would be particularly interested in seeing a long-term study of people who took molnupiravir to continue to monitor this potential effect over the next 10 or 20 years.\u003c/p>\n\u003cp>“This thing is going to go into thousands of people. And are we just going to ignore the fact that there’s this potential risk?” he said. “The risk could be zero. It could be no worse than going to get a dental X-ray — or it could do something more. But unless we find out, you know, we’re going to learn this lesson the hard way, way later than we should.”\u003c/p>\n\u003ch3>What might the new antivirals mean for cancer patients?\u003c/h3>\n\u003cp>Because the new antiviral Pfizer is developing is a protease inhibitor, infectious disease specialists are familiar with how it works. So we already know: These drugs have the potential to interfere with many therapies used to treat cancer, Tobias Hohl, chief of the infectious diseases service at Memorial Sloan Kettering Cancer Center in New York, told STAT.\u003c/p>\n\u003cp>“They’re going to be very helpful [in our] armamentarium, but they will not substitute for prevention or vaccination efforts because these are not medicines that are completely benign and harmless in terms of their drug-drug interactions and toxicity,” he said. “So we’re going to have to be careful and thoughtful about how we use our protease inhibitors.”\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>Matthew Herper, Damian Garde, Kate Sheridan, Adam Feuerstein, Andrew Joseph, and Elizabeth Cooney contributed reporting.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"title": "Mixing and Matching COVID Vaccines: What We Know",
"headTitle": "Mixing and Matching COVID Vaccines: What We Know | KQED",
"content": "\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">L\u003c/span>\u003c/span>ater this week an expert committee that advises the Centers for Disease Control and Prevention will hear about the results of a clinical trial that could influence how COVID-19 vaccines are used in this country at some point in the future. The trial, conducted by the National Institute of Allergy and Infectious Diseases, is a so-called mix-and-match trial, testing the vaccines authorized in the U.S. in combinations with each other.\u003c/p>\n\u003cp>The goal of the trial was to see whether using a different vaccine as a booster shot improves protection. So does getting a dose of Pfizer vaccine after getting a single dose of Johnson & Johnson’s vaccine trigger production of more antibodies than a second dose of the J&J would? Are the messenger RNA vaccines made by Pfizer and Moderna virtually interchangeable, or does switching produce a broader set of immune responses?\u003c/p>\n\u003cp>This isn’t theoretical. The booster shot most vaccinated Americans are in the process of getting or booking may not be the last needed. Figuring out how to optimize use of the current generation of COVID-19 vaccines is critical, a number of experts have told STAT.\u003c/p>\n\u003cp>Michael Osterholm, director of the University of Minnesota’s Center for Infectious Diseases Research and Policy, said we need to realize that many questions remain to be answered about use of these vaccines. We don’t know the optimal dose. We don’t know the most effective interval between doses. We don’t know how many doses we’re going to need and we don’t know whether we would get more durable protection if we mix up the vaccines each person receives, he said.\u003c/p>\n\u003cp>In terms of how we use COVID-19 vaccines, we’re in the very early days, Osterholm said, adding that now that we have effective vaccines, we need to start figuring out how best to use them. “We have to start adopting a public health mindset for decision making,” he said.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>What follows is a primer on what we know about mixing COVID-19 vaccines.\u003c/p>\n\u003ch3>Let’s start with the terminology\u003c/h3>\n\u003cp>If you get a booster jab that is of the same brand as your previous jab or jabs, you are getting a \u003cem>homologous \u003c/em>booster. In the United States, most people who have been vaccinated have had homologous vaccine series and homologous boosters.\u003c/p>\n\u003cp>There may be some exceptions. Earlier in the vaccine rollout, when supplies were scarce, the CDC advised that people could be given a second shot of whatever vaccine was on hand if they were due for their second shot of vaccine and no supplies of the brand they were due to get were available.\u003c/p>\n\u003cp>If your original series of vaccines or the booster were from different manufacturers, you have what’s called a \u003cem>heterologous\u003c/em> vaccine series or a heterologous boost.\u003c/p>\n\u003cp>A few vaccines are actually designed to capture the benefits of heterologous boosting. For instance, Johnson & Johnson’s Ebola vaccine uses two different types of vaccines — one of which is made using a similar design to the company’s COVID-19 vaccine. Likewise, the Sputnik V vaccine is made up of two doses of similar but not identical vaccines, each made using a different adenovirus that has been modified to carry genetic material from the SARS-CoV-2 virus. In both cases, the goal was to ensure that the immune response the first dose generated didn’t prevent the second shot from taking effect.\u003c/p>\n\u003ch3>Necessity is the mother of invention\u003c/h3>\n\u003cp>As mentioned above, most immunized people in the United States were vaccinated with a homologous series of vaccines. But elsewhere heterologous regimens were used for a couple of different reasons.\u003c/p>\n\u003cp>In the early days of the vaccine rollout, some countries opted to use heterologous boosts because they didn’t have adequate supply to be able to give people a matching shot when they were due for their second dose. And after the AstraZeneca vaccine was seen to cause serious clotting problems in some people who received it (a problem later seen with the J&J vaccine too), some countries stopped using it or limited its use to older adults, for whom the risk of a clotting event after vaccination appeared to be lower. Younger adults were offered one of the mRNA vaccines as their second dose instead.\u003c/p>\n\u003cp>Kathryn Edwards, a vaccines researcher at Vanderbilt University, suggested the United States should probably look at whether specific brands of booster doses should be targeted at certain populations — or more specifically, if certain people should be steered away from certain vaccines when it comes time for them to get boosters. With concerns about myocarditis in young males associated with mRNA vaccines and clotting problems reported mainly with younger women who got one of the viral vectored vaccines, such as the J&J, maybe it’s time to think about who gets which type of COVID-19 vaccine, Edwards said.\u003c/p>\n\u003ch3>A natural experiment turns into a border barrier\u003c/h3>\n\u003cp>Countries like the United Kingdom, Canada, France, and Germany that used heterologous vaccine approaches have created a travel conundrum for their citizens.\u003c/p>\n\u003cp>A number of countries — the United States among them — do not consider people who received two different brands of vaccines fully vaccinated, even if the person’s home country does. This means someone who got an mRNA vaccine as a second dose after receiving an AstraZeneca shot as a priming dose is not deemed fully vaccinated and is not eligible to travel to the U.S. or other countries with the same rule.\u003c/p>\n\u003cp>Canada has roughly 4 million people who were vaccinated on a heterologous schedule. The U.S. and its northern neighbor share the world’s longest border and in pre-Covid times, travel across it was brisk. Now many Canadians are in limbo, unsure if or when they will be allowed to cross into the U.S.\u003c/p>\n\u003cp>Figuring out how to deal with a range of vaccines used in a variety of ways around the world is going to be a challenge that the Biden administration and other governments will have to grapple with as international travel increases.\u003c/p>\n\u003ch3>All combos may not be created equal\u003c/h3>\n\u003cp>Is it possible that any combination of vaccine types or brands will work as well — or better — than if the shots were all of a single brand? That’s not yet clear, but it’s possible — even likely — that the combinations and the order in which the vaccines are given will matter.\u003c/p>\n\u003cp>“A followed by B may not be the same as B followed by A,” explained Bruce Gellin, chief of global public health strategy for the Rockefeller Foundation’s pandemic prevention institute.\u003c/p>\n\u003cp>A number of small studies done in Europe have shown that following up AstraZeneca’s adenovirus-vectored vaccine with a Pfizer or a \u003ca href=\"https://www.nejm.org/doi/10.1056/NEJMc2110716\" target=\"_blank\" rel=\"noopener noreferrer\">Moderna\u003c/a> mRNA booster elicits a greater immune response than what is seen from two doses of the AstraZeneca alone. But an ongoing research effort at Britain’s University of Oxford comparing COVID-19 vaccine combinations called the Com-CoV trials suggests that the inverse may not be true.\u003c/p>\n\u003cp>Scientists conducting the original \u003ca href=\"https://www.thelancet.com/action/showPdf?pii=S0140-6736%2821%2901694-9\" target=\"_blank\" rel=\"noopener noreferrer\">Com-CoV trial\u003c/a> gave volunteers two doses apiece of either AstraZeneca or Pfizer, comparing the antibody levels those regimens elicited to AstraZeneca followed by Pfizer or Pfizer followed by AstraZeneca. Pfizer after AstraZeneca generated higher antibody levels than two doses of AstraZeneca alone; but AstraZeneca after Pfizer was not better than two doses of Pfizer.\u003c/p>\n\u003cp>“The priming event is really important,” said \u003ca href=\"https://www.statnews.com/2021/09/13/barney-graham-leaves-nih-vaccine-research-center/\">Barney Graham\u003c/a>, who was deputy director of the National Institutes of Health’s Vaccine Research Center until the end of August and who played a critical role in the design of the Moderna and other vaccine prototypes.\u003c/p>\n\u003cp>Graham explained that the kind of immune response one gets from COVID-19 vaccines is determined by the first dose. “And so it kind of locks you into a repertoire and a pattern of antibody, T-cell balances that carry on through subsequent boosters,” he said.\u003c/p>\n\u003cp>Much remains to be learned about how to effectively mix COVID-19 vaccines — and it will take time to answer these questions, Graham said. “Those are the kind of things that happen over a 12-year development program. We didn’t do that this time.”\u003c/p>\n\u003ch3>Mixed vaccines carry a punch\u003c/h3>\n\u003cp>In general, COVID-19 vaccines are what’s known as reactogenic; they can carry a wallop. Fevers, sore arms, fatigue, and malaise — a lot of people report feeling kind of crappy in the hours or even day or two after getting a shot.\u003c/p>\n\u003cp>Complaints about reactogenicity were even greater among people who got mixed vaccine brands, the \u003ca href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01115-6/fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">Com-CoV trial\u003c/a> reported. So, potentially more post-vaccination side effects, but nothing unmanageable. “It is reassuring that all reactogenicity symptoms were short lived,” the Com-CoV researchers said in a short study published in late May in The Lancet.\u003c/p>\n\u003ch3>The challenge ahead\u003c/h3>\n\u003cp>If evidence continues to amass suggesting that mixing vaccine brands would be of benefit, how do those data get translated into public policy? That won’t be easy, experts warn.\u003c/p>\n\u003cp>Typically, regulators like the Food and Drug Administration act on requests from companies. They review data provided by a manufacturer and decide yes, this vaccine or drug can be given to these people or no, it should not be.\u003c/p>\n\u003cp>But when you are talking about a plan that involves combining products from two different companies, things become much more complex. None of these companies have asked to have a rival’s vaccine used as a booster for their COVID-19 shot — and they’re not likely to.\u003c/p>\n\u003cp>“Normally the manufacturer puts in an application to do something,” said Glen Nowak, director of the Center for Health and Risk Communication at Grady College of Journalism and Mass Communication. “Who then has that responsibility to bring forward a recommendation to mix and match? I think it’s a very good question.”\u003c/p>\n\u003cp>The CDC could address the issue, said Norman Baylor, president and CEO of Biologics Consulting and a former head of the FDA’s Office of Vaccines. Its advisory panel, ACIP, could evaluate the data and, if it supports using heterologous boosts, recommend that this is the way the vaccines could be used. Such advice could take the form of what is known as preferential recommendations — effectively not saying that vaccine B must be used after vaccine A, but noting it would be advisable to do so.\u003c/p>\n\u003cp>Could that happen? Possibly. But if it does happen, it will likely affect the way COVID-19 vaccines are used in the future — in people who haven’t yet started to be vaccinated, or if and when people in the country need a fourth dose of vaccine. Because by the time there are enough data to move forward with this type of policy, most Americans who are currently due for a booster jab will likely have had one.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003ci data-stringify-type=\"italic\">This story was originally published by \u003c/i>\u003ci data-stringify-type=\"italic\">\u003ca class=\"c-link\" href=\"https://www.statnews.com/2021/10/12/a-primer-on-what-we-know-about-mixing-and-matching-covid-vaccines/?utm_content=bufferd53a2&utm_medium=social&utm_source=facebook&utm_campaign=facebook_organic\" target=\"_blank\" rel=\"noopener noreferrer\" data-stringify-link=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" data-sk=\"tooltip_parent\" data-remove-tab-index=\"true\">STAT\u003c/a>\u003c/i>\u003ci data-stringify-type=\"italic\">, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/i>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">L\u003c/span>\u003c/span>ater this week an expert committee that advises the Centers for Disease Control and Prevention will hear about the results of a clinical trial that could influence how COVID-19 vaccines are used in this country at some point in the future. The trial, conducted by the National Institute of Allergy and Infectious Diseases, is a so-called mix-and-match trial, testing the vaccines authorized in the U.S. in combinations with each other.\u003c/p>\n\u003cp>The goal of the trial was to see whether using a different vaccine as a booster shot improves protection. So does getting a dose of Pfizer vaccine after getting a single dose of Johnson & Johnson’s vaccine trigger production of more antibodies than a second dose of the J&J would? Are the messenger RNA vaccines made by Pfizer and Moderna virtually interchangeable, or does switching produce a broader set of immune responses?\u003c/p>\n\u003cp>This isn’t theoretical. The booster shot most vaccinated Americans are in the process of getting or booking may not be the last needed. Figuring out how to optimize use of the current generation of COVID-19 vaccines is critical, a number of experts have told STAT.\u003c/p>\n\u003cp>Michael Osterholm, director of the University of Minnesota’s Center for Infectious Diseases Research and Policy, said we need to realize that many questions remain to be answered about use of these vaccines. We don’t know the optimal dose. We don’t know the most effective interval between doses. We don’t know how many doses we’re going to need and we don’t know whether we would get more durable protection if we mix up the vaccines each person receives, he said.\u003c/p>\n\u003cp>In terms of how we use COVID-19 vaccines, we’re in the very early days, Osterholm said, adding that now that we have effective vaccines, we need to start figuring out how best to use them. “We have to start adopting a public health mindset for decision making,” he said.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>What follows is a primer on what we know about mixing COVID-19 vaccines.\u003c/p>\n\u003ch3>Let’s start with the terminology\u003c/h3>\n\u003cp>If you get a booster jab that is of the same brand as your previous jab or jabs, you are getting a \u003cem>homologous \u003c/em>booster. In the United States, most people who have been vaccinated have had homologous vaccine series and homologous boosters.\u003c/p>\n\u003cp>There may be some exceptions. Earlier in the vaccine rollout, when supplies were scarce, the CDC advised that people could be given a second shot of whatever vaccine was on hand if they were due for their second shot of vaccine and no supplies of the brand they were due to get were available.\u003c/p>\n\u003cp>If your original series of vaccines or the booster were from different manufacturers, you have what’s called a \u003cem>heterologous\u003c/em> vaccine series or a heterologous boost.\u003c/p>\n\u003cp>A few vaccines are actually designed to capture the benefits of heterologous boosting. For instance, Johnson & Johnson’s Ebola vaccine uses two different types of vaccines — one of which is made using a similar design to the company’s COVID-19 vaccine. Likewise, the Sputnik V vaccine is made up of two doses of similar but not identical vaccines, each made using a different adenovirus that has been modified to carry genetic material from the SARS-CoV-2 virus. In both cases, the goal was to ensure that the immune response the first dose generated didn’t prevent the second shot from taking effect.\u003c/p>\n\u003ch3>Necessity is the mother of invention\u003c/h3>\n\u003cp>As mentioned above, most immunized people in the United States were vaccinated with a homologous series of vaccines. But elsewhere heterologous regimens were used for a couple of different reasons.\u003c/p>\n\u003cp>In the early days of the vaccine rollout, some countries opted to use heterologous boosts because they didn’t have adequate supply to be able to give people a matching shot when they were due for their second dose. And after the AstraZeneca vaccine was seen to cause serious clotting problems in some people who received it (a problem later seen with the J&J vaccine too), some countries stopped using it or limited its use to older adults, for whom the risk of a clotting event after vaccination appeared to be lower. Younger adults were offered one of the mRNA vaccines as their second dose instead.\u003c/p>\n\u003cp>Kathryn Edwards, a vaccines researcher at Vanderbilt University, suggested the United States should probably look at whether specific brands of booster doses should be targeted at certain populations — or more specifically, if certain people should be steered away from certain vaccines when it comes time for them to get boosters. With concerns about myocarditis in young males associated with mRNA vaccines and clotting problems reported mainly with younger women who got one of the viral vectored vaccines, such as the J&J, maybe it’s time to think about who gets which type of COVID-19 vaccine, Edwards said.\u003c/p>\n\u003ch3>A natural experiment turns into a border barrier\u003c/h3>\n\u003cp>Countries like the United Kingdom, Canada, France, and Germany that used heterologous vaccine approaches have created a travel conundrum for their citizens.\u003c/p>\n\u003cp>A number of countries — the United States among them — do not consider people who received two different brands of vaccines fully vaccinated, even if the person’s home country does. This means someone who got an mRNA vaccine as a second dose after receiving an AstraZeneca shot as a priming dose is not deemed fully vaccinated and is not eligible to travel to the U.S. or other countries with the same rule.\u003c/p>\n\u003cp>Canada has roughly 4 million people who were vaccinated on a heterologous schedule. The U.S. and its northern neighbor share the world’s longest border and in pre-Covid times, travel across it was brisk. Now many Canadians are in limbo, unsure if or when they will be allowed to cross into the U.S.\u003c/p>\n\u003cp>Figuring out how to deal with a range of vaccines used in a variety of ways around the world is going to be a challenge that the Biden administration and other governments will have to grapple with as international travel increases.\u003c/p>\n\u003ch3>All combos may not be created equal\u003c/h3>\n\u003cp>Is it possible that any combination of vaccine types or brands will work as well — or better — than if the shots were all of a single brand? That’s not yet clear, but it’s possible — even likely — that the combinations and the order in which the vaccines are given will matter.\u003c/p>\n\u003cp>“A followed by B may not be the same as B followed by A,” explained Bruce Gellin, chief of global public health strategy for the Rockefeller Foundation’s pandemic prevention institute.\u003c/p>\n\u003cp>A number of small studies done in Europe have shown that following up AstraZeneca’s adenovirus-vectored vaccine with a Pfizer or a \u003ca href=\"https://www.nejm.org/doi/10.1056/NEJMc2110716\" target=\"_blank\" rel=\"noopener noreferrer\">Moderna\u003c/a> mRNA booster elicits a greater immune response than what is seen from two doses of the AstraZeneca alone. But an ongoing research effort at Britain’s University of Oxford comparing COVID-19 vaccine combinations called the Com-CoV trials suggests that the inverse may not be true.\u003c/p>\n\u003cp>Scientists conducting the original \u003ca href=\"https://www.thelancet.com/action/showPdf?pii=S0140-6736%2821%2901694-9\" target=\"_blank\" rel=\"noopener noreferrer\">Com-CoV trial\u003c/a> gave volunteers two doses apiece of either AstraZeneca or Pfizer, comparing the antibody levels those regimens elicited to AstraZeneca followed by Pfizer or Pfizer followed by AstraZeneca. Pfizer after AstraZeneca generated higher antibody levels than two doses of AstraZeneca alone; but AstraZeneca after Pfizer was not better than two doses of Pfizer.\u003c/p>\n\u003cp>“The priming event is really important,” said \u003ca href=\"https://www.statnews.com/2021/09/13/barney-graham-leaves-nih-vaccine-research-center/\">Barney Graham\u003c/a>, who was deputy director of the National Institutes of Health’s Vaccine Research Center until the end of August and who played a critical role in the design of the Moderna and other vaccine prototypes.\u003c/p>\n\u003cp>Graham explained that the kind of immune response one gets from COVID-19 vaccines is determined by the first dose. “And so it kind of locks you into a repertoire and a pattern of antibody, T-cell balances that carry on through subsequent boosters,” he said.\u003c/p>\n\u003cp>Much remains to be learned about how to effectively mix COVID-19 vaccines — and it will take time to answer these questions, Graham said. “Those are the kind of things that happen over a 12-year development program. We didn’t do that this time.”\u003c/p>\n\u003ch3>Mixed vaccines carry a punch\u003c/h3>\n\u003cp>In general, COVID-19 vaccines are what’s known as reactogenic; they can carry a wallop. Fevers, sore arms, fatigue, and malaise — a lot of people report feeling kind of crappy in the hours or even day or two after getting a shot.\u003c/p>\n\u003cp>Complaints about reactogenicity were even greater among people who got mixed vaccine brands, the \u003ca href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01115-6/fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">Com-CoV trial\u003c/a> reported. So, potentially more post-vaccination side effects, but nothing unmanageable. “It is reassuring that all reactogenicity symptoms were short lived,” the Com-CoV researchers said in a short study published in late May in The Lancet.\u003c/p>\n\u003ch3>The challenge ahead\u003c/h3>\n\u003cp>If evidence continues to amass suggesting that mixing vaccine brands would be of benefit, how do those data get translated into public policy? That won’t be easy, experts warn.\u003c/p>\n\u003cp>Typically, regulators like the Food and Drug Administration act on requests from companies. They review data provided by a manufacturer and decide yes, this vaccine or drug can be given to these people or no, it should not be.\u003c/p>\n\u003cp>But when you are talking about a plan that involves combining products from two different companies, things become much more complex. None of these companies have asked to have a rival’s vaccine used as a booster for their COVID-19 shot — and they’re not likely to.\u003c/p>\n\u003cp>“Normally the manufacturer puts in an application to do something,” said Glen Nowak, director of the Center for Health and Risk Communication at Grady College of Journalism and Mass Communication. “Who then has that responsibility to bring forward a recommendation to mix and match? I think it’s a very good question.”\u003c/p>\n\u003cp>The CDC could address the issue, said Norman Baylor, president and CEO of Biologics Consulting and a former head of the FDA’s Office of Vaccines. Its advisory panel, ACIP, could evaluate the data and, if it supports using heterologous boosts, recommend that this is the way the vaccines could be used. Such advice could take the form of what is known as preferential recommendations — effectively not saying that vaccine B must be used after vaccine A, but noting it would be advisable to do so.\u003c/p>\n\u003cp>Could that happen? Possibly. But if it does happen, it will likely affect the way COVID-19 vaccines are used in the future — in people who haven’t yet started to be vaccinated, or if and when people in the country need a fourth dose of vaccine. Because by the time there are enough data to move forward with this type of policy, most Americans who are currently due for a booster jab will likely have had one.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003ci data-stringify-type=\"italic\">This story was originally published by \u003c/i>\u003ci data-stringify-type=\"italic\">\u003ca class=\"c-link\" href=\"https://www.statnews.com/2021/10/12/a-primer-on-what-we-know-about-mixing-and-matching-covid-vaccines/?utm_content=bufferd53a2&utm_medium=social&utm_source=facebook&utm_campaign=facebook_organic\" target=\"_blank\" rel=\"noopener noreferrer\" data-stringify-link=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" data-sk=\"tooltip_parent\" data-remove-tab-index=\"true\">STAT\u003c/a>\u003c/i>\u003ci data-stringify-type=\"italic\">, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/i>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>The \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">announcement\u003c/a> that a pill from Merck and partner Ridgeback Biotherapeutics kept COVID-19 patients out of the hospital made headlines and moved stocks. But as is so often true when data are released by press release, there are still many questions left unanswered.\u003c/p>\n\u003cp>Doctors are excited about the medicine, molnupiravir, because a regimen of pills, even one that involves taking several pills twice a day for five days, should be far easier to deliver to patients than current antiviral COVID-19 treatments, which must be given intravenously. But it’s still unclear how widely this treatment will be used. There will also be debate among financial analysts at investment banks regarding exactly how many billions of dollars in sales the new drug will generate.\u003c/p>\n\u003cp>The drugmaker \u003ca href=\"https://www.npr.org/2021/10/11/1045005513/merck-asks-fda-to-authorize-promising-anti-covid-pill\" target=\"_blank\" rel=\"noopener noreferrer\">asked\u003c/a> U.S. regulators Monday to authorize its pill against COVID-19 in what could add an easy-to-use weapon to the world’s arsenal against the pandemic.\u003c/p>\n\u003cp>Here are some things to keep in mind as we learn more about molnupiravir and about other COVID-19 fighting pills in development at other companies.\u003c/p>\n\u003ch3>How many other anti-COVID pills will end up proving effective?\u003c/h3>\n\u003cp>One of the reasons that the success of molnupiravir is such a big deal is that there were questions as to whether an antiviral pill could help COVID-19 patients if given early enough. This medicine certainly did, reducing hospitalizations by 50%; it also appeared to have an impact on whether patients survived. That makes it a game-changer. Its success also ups the odds that other medicines will prove effective, too.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Results for other drugs are likely to be released by the end of the year. That includes data about a similar pill, also given as a five-day course, from Atea Pharmaceuticals and Roche, and about a pill developed by Pfizer that is from a different drug class and might be combined with molnupiravir.\u003c/p>\n\u003cp>Another positive note for all these drugs: remdesivir, the intravenous antiviral made by Gilead Sciences, also showed positive results when used for three days after onset of symptoms. That’s not practical — it had to be given via IV for three days — but bodes well for antiviral pills showing some efficacy. It’s even possible those pills might be combined.\u003c/p>\n\u003ch3>How safe is molnupiravir?\u003c/h3>\n\u003cp>Obviously, a drug given early in COVID needs a clean safety profile. So far, the data included in the press release look very good. Patients in the placebo arm were three times more likely to withdraw from the study due to apparent side effects than those who actually received molnupiravir. That likely means the side effects of COVID were worse than those of the drug.\u003c/p>\n\u003cp>But only so much can be seen from that kind of data. Molnupiravir works by messing up the way the virus copies RNA, its genetic material, preventing viral replication. There is some concern it could be mutagenic, meaning that it could cause mutations. One result could be that it causes birth defects. In the clinical trial, both women and men were told to either abstain from sexual intercourse or to use contraception while they were taking the drug and for at least four days after. Women of childbearing age also needed a negative pregnancy test to start taking the medicine.\u003c/p>\n\u003ch3>Could there be other effects?\u003c/h3>\n\u003cp>In a conference call with reporters, Daria Hazuda, a top Merck virologist, said that Merck and Ridgeback had studied the mutagenic potential of the drug in both cell lines and in animal models that are routinely used in drug development and which are accepted by regulatory agencies.\u003c/p>\n\u003cp>“I would say that in all of the models where we have looked, we have seen no evidence of the potential for mutagenicity for this agent,” Hazuda said. “We’re very comfortable that the drug will be safe if used as intended and at the concentrations where we have looked and in the concentrations which we are achieving in patients.”\u003c/p>\n\u003ch2>Will molnupiravir be used only in unvaccinated patients?\u003c/h2>\n\u003cp>Merck’s trial was conducted entirely in patients who had not been vaccinated. That made it much easier to show that the medicine can reduce hospitalization and death — because patients who have not previously been vaccinated are more likely to be hospitalized or die.\u003c/p>\n\u003cp>But does that mean that, in practice, the drug will only be used in unvaccinated patients, or will it be used in cases of breakthrough infections? It’s hard to say. Patients with breakthrough infections are at lower risk of hospitalization, which could change the risk-benefit calculus around the medicine.\u003c/p>\n\u003ch3>So how big will the market be?\u003c/h3>\n\u003cp>Daina Graybosch, an analyst at SVB Leerink, forecast in a note to investors that molnupiravir sales will peak near $5 billion a year in 2022.\u003c/p>\n\u003cp>Built into this are a number of assumptions, among them that the first-mover advantage will mean that Merck and Ridgeback will be used more than the other pills in development and that vaccinated patients with breakthrough infections will be eligible to receive the drug, too.\u003c/p>\n\u003cp>Timothy Anderson of Wolfe Research, a standalone equities research firm, takes the other side, essentially saying it is too soon to put a number on molnupiravir sales, in part because data from competing firms are not available but also because other questions remain.\u003c/p>\n\u003cp>“Vaccination rates continue to rise in the US and other developed markets, meaning the cohort of patients who would qualify for molnupiravir (i.e. mostly those who are unvaccinated, at higher risk) will shrink over time,” Anderson wrote in a note to clients.\u003c/p>\n\u003cp>Successfully using the drug, he pointed out, will also require that patients get tested early in their disease course. If people start to skip getting tested, they won’t receive molnupiravir.\u003c/p>\n\u003ch3>What will it cost and who will pay?\u003c/h3>\n\u003cp>Most analysts are basing the cost of molnupiravir on the $1.2 billion the U.S. government spent to lock up 1.7 million courses of the medicine, which works out to $700 per five day course. But Anderson points out that the cost for a new pill to treat influenza developed by Roche is just $150 per course. Will the $700 price hold up?\u003c/p>\n\u003cp>Questions about payment and distribution could play a big role in how big the market for molnupiravir gets. Anderson assumes in his note to clients that, in the U.S., insurance companies will be paying for the drug through traditional channels. He expects that at $700, insurers will restrict use of the drug to those who are unvaccinated and have multiple risk factors for disease — basically similar profiles to those who are in the trials.\u003c/p>\n\u003cp>But it’s also possible that sales in the U.S. might be mostly to the government. This is how things have worked with both remdesivir, used in hospitalized patients, and the monoclonal antibodies developed by Regeneron and Eli Lilly. Will the government handle the distribution of a pill granted an emergency use authorization in the same way that it has handled the monoclonals?\u003c/p>\n\u003ch3>How will the availability of COVID pills affect vaccines and other treatments?\u003c/h3>\n\u003cp>It doesn’t make any sense to forego a COVID vaccine because a pill to treat the disease exists. The benefits are additive, and someone who got a breakthrough infection and then the pill has a much lower risk of hospitalization than someone who just relied on the pill.\u003c/p>\n\u003cp>But it seems likely that some people will feel less urgency to get vaccinated as a result of molnupiravir’s existence, and shares in Pfizer, BioNTech, and Moderna all fell on Friday. The latter two are down again Monday morning.\u003c/p>\n\u003cp>Shares in Regeneron also fell, as oral drugs create uncertainty for its monoclonal antibody treatment for COVID. The landscape there is uncertain, with other companies coming forward with antibodies that may have advantages. One small firm, Adagio Therapeutics, recently presented early data on an antibody it thinks could be given as a single shot.\u003c/p>\n\u003ch3>How does this treatment relate to ivermectin?\u003c/h3>\n\u003cp>This is simple: it doesn’t. But it’s worth taking a look at what data are available for each.\u003c/p>\n\u003cp>Ivermectin, ironically, is another Merck drug. The company’s donation of the medicine to be used to combat a parasitic disease called river blindness is one of the great examples of pharmaceutical philanthropy. It’s also used as a veterinary drug to treat heartworm.\u003c/p>\n\u003cp>Early in the pandemic, there were studies in cell cultures that showed that ivermectin and another drug, hydroxychloroquine, might be worth testing as COVID-19 treatments. Multiple studies have failed to show a benefit for hydroxychloroquine, but the picture is murkier for ivermectin. Still, one of the largest studies showing a benefit was \u003ca href=\"https://www.nature.com/articles/d41586-021-02081-w\" target=\"_blank\" rel=\"noopener noreferrer\">withdrawn due to widespread flaws\u003c/a>.\u003c/p>\n\u003cp>There is a study conducted in Brazil, the Together Trial, that tested a three-day course of ivermectin compared to placebo and showed there \u003ca href=\"https://elemental.medium.com/ivermectin-for-covid-19-an-update-5e913bb49483\" target=\"_blank\" rel=\"noopener noreferrer\">was no benefit on hospitalizations and ER visits\u003c/a>. That would make it unlikely that ivermectin, an old antiparasitic, would have efficacy approaching this newer antiviral.\u003c/p>\n\u003cp>Drug companies are unlikely to conduct large, rigorous studies of older generic medicines — although Novartis did begin, then stop, a hydroxychloroquine study. But right now it is unlikely that ivermectin is the oral COVID medicine the world needs. Molnupiravir, on the other hand, might be.\u003c/p>\n\u003caside class=\"read-more donate\">\u003c/aside>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The \u003ca href=\"https://www.statnews.com/2021/10/01/mercks-antiviral-pill-reduces-hospitalization-of-covid-patients-a-possible-game-changer-for-treatment/\" target=\"_blank\" rel=\"noopener noreferrer\">announcement\u003c/a> that a pill from Merck and partner Ridgeback Biotherapeutics kept COVID-19 patients out of the hospital made headlines and moved stocks. But as is so often true when data are released by press release, there are still many questions left unanswered.\u003c/p>\n\u003cp>Doctors are excited about the medicine, molnupiravir, because a regimen of pills, even one that involves taking several pills twice a day for five days, should be far easier to deliver to patients than current antiviral COVID-19 treatments, which must be given intravenously. But it’s still unclear how widely this treatment will be used. There will also be debate among financial analysts at investment banks regarding exactly how many billions of dollars in sales the new drug will generate.\u003c/p>\n\u003cp>The drugmaker \u003ca href=\"https://www.npr.org/2021/10/11/1045005513/merck-asks-fda-to-authorize-promising-anti-covid-pill\" target=\"_blank\" rel=\"noopener noreferrer\">asked\u003c/a> U.S. regulators Monday to authorize its pill against COVID-19 in what could add an easy-to-use weapon to the world’s arsenal against the pandemic.\u003c/p>\n\u003cp>Here are some things to keep in mind as we learn more about molnupiravir and about other COVID-19 fighting pills in development at other companies.\u003c/p>\n\u003ch3>How many other anti-COVID pills will end up proving effective?\u003c/h3>\n\u003cp>One of the reasons that the success of molnupiravir is such a big deal is that there were questions as to whether an antiviral pill could help COVID-19 patients if given early enough. This medicine certainly did, reducing hospitalizations by 50%; it also appeared to have an impact on whether patients survived. That makes it a game-changer. Its success also ups the odds that other medicines will prove effective, too.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Results for other drugs are likely to be released by the end of the year. That includes data about a similar pill, also given as a five-day course, from Atea Pharmaceuticals and Roche, and about a pill developed by Pfizer that is from a different drug class and might be combined with molnupiravir.\u003c/p>\n\u003cp>Another positive note for all these drugs: remdesivir, the intravenous antiviral made by Gilead Sciences, also showed positive results when used for three days after onset of symptoms. That’s not practical — it had to be given via IV for three days — but bodes well for antiviral pills showing some efficacy. It’s even possible those pills might be combined.\u003c/p>\n\u003ch3>How safe is molnupiravir?\u003c/h3>\n\u003cp>Obviously, a drug given early in COVID needs a clean safety profile. So far, the data included in the press release look very good. Patients in the placebo arm were three times more likely to withdraw from the study due to apparent side effects than those who actually received molnupiravir. That likely means the side effects of COVID were worse than those of the drug.\u003c/p>\n\u003cp>But only so much can be seen from that kind of data. Molnupiravir works by messing up the way the virus copies RNA, its genetic material, preventing viral replication. There is some concern it could be mutagenic, meaning that it could cause mutations. One result could be that it causes birth defects. In the clinical trial, both women and men were told to either abstain from sexual intercourse or to use contraception while they were taking the drug and for at least four days after. Women of childbearing age also needed a negative pregnancy test to start taking the medicine.\u003c/p>\n\u003ch3>Could there be other effects?\u003c/h3>\n\u003cp>In a conference call with reporters, Daria Hazuda, a top Merck virologist, said that Merck and Ridgeback had studied the mutagenic potential of the drug in both cell lines and in animal models that are routinely used in drug development and which are accepted by regulatory agencies.\u003c/p>\n\u003cp>“I would say that in all of the models where we have looked, we have seen no evidence of the potential for mutagenicity for this agent,” Hazuda said. “We’re very comfortable that the drug will be safe if used as intended and at the concentrations where we have looked and in the concentrations which we are achieving in patients.”\u003c/p>\n\u003ch2>Will molnupiravir be used only in unvaccinated patients?\u003c/h2>\n\u003cp>Merck’s trial was conducted entirely in patients who had not been vaccinated. That made it much easier to show that the medicine can reduce hospitalization and death — because patients who have not previously been vaccinated are more likely to be hospitalized or die.\u003c/p>\n\u003cp>But does that mean that, in practice, the drug will only be used in unvaccinated patients, or will it be used in cases of breakthrough infections? It’s hard to say. Patients with breakthrough infections are at lower risk of hospitalization, which could change the risk-benefit calculus around the medicine.\u003c/p>\n\u003ch3>So how big will the market be?\u003c/h3>\n\u003cp>Daina Graybosch, an analyst at SVB Leerink, forecast in a note to investors that molnupiravir sales will peak near $5 billion a year in 2022.\u003c/p>\n\u003cp>Built into this are a number of assumptions, among them that the first-mover advantage will mean that Merck and Ridgeback will be used more than the other pills in development and that vaccinated patients with breakthrough infections will be eligible to receive the drug, too.\u003c/p>\n\u003cp>Timothy Anderson of Wolfe Research, a standalone equities research firm, takes the other side, essentially saying it is too soon to put a number on molnupiravir sales, in part because data from competing firms are not available but also because other questions remain.\u003c/p>\n\u003cp>“Vaccination rates continue to rise in the US and other developed markets, meaning the cohort of patients who would qualify for molnupiravir (i.e. mostly those who are unvaccinated, at higher risk) will shrink over time,” Anderson wrote in a note to clients.\u003c/p>\n\u003cp>Successfully using the drug, he pointed out, will also require that patients get tested early in their disease course. If people start to skip getting tested, they won’t receive molnupiravir.\u003c/p>\n\u003ch3>What will it cost and who will pay?\u003c/h3>\n\u003cp>Most analysts are basing the cost of molnupiravir on the $1.2 billion the U.S. government spent to lock up 1.7 million courses of the medicine, which works out to $700 per five day course. But Anderson points out that the cost for a new pill to treat influenza developed by Roche is just $150 per course. Will the $700 price hold up?\u003c/p>\n\u003cp>Questions about payment and distribution could play a big role in how big the market for molnupiravir gets. Anderson assumes in his note to clients that, in the U.S., insurance companies will be paying for the drug through traditional channels. He expects that at $700, insurers will restrict use of the drug to those who are unvaccinated and have multiple risk factors for disease — basically similar profiles to those who are in the trials.\u003c/p>\n\u003cp>But it’s also possible that sales in the U.S. might be mostly to the government. This is how things have worked with both remdesivir, used in hospitalized patients, and the monoclonal antibodies developed by Regeneron and Eli Lilly. Will the government handle the distribution of a pill granted an emergency use authorization in the same way that it has handled the monoclonals?\u003c/p>\n\u003ch3>How will the availability of COVID pills affect vaccines and other treatments?\u003c/h3>\n\u003cp>It doesn’t make any sense to forego a COVID vaccine because a pill to treat the disease exists. The benefits are additive, and someone who got a breakthrough infection and then the pill has a much lower risk of hospitalization than someone who just relied on the pill.\u003c/p>\n\u003cp>But it seems likely that some people will feel less urgency to get vaccinated as a result of molnupiravir’s existence, and shares in Pfizer, BioNTech, and Moderna all fell on Friday. The latter two are down again Monday morning.\u003c/p>\n\u003cp>Shares in Regeneron also fell, as oral drugs create uncertainty for its monoclonal antibody treatment for COVID. The landscape there is uncertain, with other companies coming forward with antibodies that may have advantages. One small firm, Adagio Therapeutics, recently presented early data on an antibody it thinks could be given as a single shot.\u003c/p>\n\u003ch3>How does this treatment relate to ivermectin?\u003c/h3>\n\u003cp>This is simple: it doesn’t. But it’s worth taking a look at what data are available for each.\u003c/p>\n\u003cp>Ivermectin, ironically, is another Merck drug. The company’s donation of the medicine to be used to combat a parasitic disease called river blindness is one of the great examples of pharmaceutical philanthropy. It’s also used as a veterinary drug to treat heartworm.\u003c/p>\n\u003cp>Early in the pandemic, there were studies in cell cultures that showed that ivermectin and another drug, hydroxychloroquine, might be worth testing as COVID-19 treatments. Multiple studies have failed to show a benefit for hydroxychloroquine, but the picture is murkier for ivermectin. Still, one of the largest studies showing a benefit was \u003ca href=\"https://www.nature.com/articles/d41586-021-02081-w\" target=\"_blank\" rel=\"noopener noreferrer\">withdrawn due to widespread flaws\u003c/a>.\u003c/p>\n\u003cp>There is a study conducted in Brazil, the Together Trial, that tested a three-day course of ivermectin compared to placebo and showed there \u003ca href=\"https://elemental.medium.com/ivermectin-for-covid-19-an-update-5e913bb49483\" target=\"_blank\" rel=\"noopener noreferrer\">was no benefit on hospitalizations and ER visits\u003c/a>. That would make it unlikely that ivermectin, an old antiparasitic, would have efficacy approaching this newer antiviral.\u003c/p>\n\u003cp>Drug companies are unlikely to conduct large, rigorous studies of older generic medicines — although Novartis did begin, then stop, a hydroxychloroquine study. But right now it is unlikely that ivermectin is the oral COVID medicine the world needs. Molnupiravir, on the other hand, might be.\u003c/p>\n\u003caside class=\"read-more donate\">\u003c/aside>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>The first results from the highly anticipated trial studying the effectiveness and safety of the Pfizer and BioNTech COVID-19 vaccine for children ages 5 to 11 showed promising results.\u003c/p>\n\u003cp>The pharmaceutical companies said early results of their trial indicate the vaccine is safe for children and establishes a strong antibody response against the virus.\u003c/p>\n\u003cp>Giving a two-dose regimen of 10 μg (micrograms) administered 21 days apart for children between 5 and 11 years old was well tolerated, according to Pfizer and BioNTech. Side effects were also generally comparable to those of people between the ages of 16 and 25 years old who received the vaccine.\u003c/p>\n\u003cp>This trial used a smaller vaccine dosage, 10 micrograms, rather than the 30 microgram dose used for people 12 and older. The dosage was selected as the preferred dose for safety and effectiveness in young children.\u003c/p>\n\u003cp>News of the results come as pediatric cases of COVID-19 are increasing amid a nationwide surge of infections.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>“Since July, pediatric cases of COVID-19 have risen by about 240 percent in the U.S. — underscoring the public health need for vaccination. These trial results provide a strong foundation for seeking authorization of our vaccine for children 5 to 11 years old, and we plan to submit them to the FDA and other regulators with urgency,” said Albert Bourla, the chairman and CEO for Pfizer.\u003c/p>\n\u003cp>“Over the past nine months, hundreds of millions of people ages 12 and older from around the world have received our COVID-19 vaccine. We are eager to extend the protection afforded by the vaccine to this younger population, subject to regulatory authorization, especially as we track the spread of the Delta variant and the substantial threat it poses to children,” Bourla said in a statement.\u003c/p>\n\u003cp>Despite the strong results, it will be some time before the general public can see an official rollout of vaccines for children ages 5 to 11. Once analysis of the trial is completed, Pfizer and BioNTech will submit the results “in the near term” to the Food and Drug Administration for review and possible emergency use authorization.\u003c/p>\n\u003cp>And even if the FDA grants that authorization, Dr. Francis Collins, director of the National Institutes of Health, recently told NPR that parents and caregivers will likely have to wait until the end of 2021 before a COVID-19 vaccine is fully approved for young children ages 5 to 11.\u003c/p>\n\u003cp>Trial results for children under 5 years of age could come later this year, the pharmaceutical companies said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“Already in March 2021, we have started the study to evaluate the immunization of younger children. Our objective was to generate and submit the data for schoolkids to regulatory authorities around the world before the winter season begins,” BioNTech CEO and co-founder Ugur Sahin said.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=COVID+Vaccine+For+Kids+Ages+5+To+11+Is+Safe+And+Effective%2C+Pfizer+Says&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The first results from the highly anticipated trial studying the effectiveness and safety of the Pfizer and BioNTech COVID-19 vaccine for children ages 5 to 11 showed promising results.\u003c/p>\n\u003cp>The pharmaceutical companies said early results of their trial indicate the vaccine is safe for children and establishes a strong antibody response against the virus.\u003c/p>\n\u003cp>Giving a two-dose regimen of 10 μg (micrograms) administered 21 days apart for children between 5 and 11 years old was well tolerated, according to Pfizer and BioNTech. Side effects were also generally comparable to those of people between the ages of 16 and 25 years old who received the vaccine.\u003c/p>\n\u003cp>This trial used a smaller vaccine dosage, 10 micrograms, rather than the 30 microgram dose used for people 12 and older. The dosage was selected as the preferred dose for safety and effectiveness in young children.\u003c/p>\n\u003cp>News of the results come as pediatric cases of COVID-19 are increasing amid a nationwide surge of infections.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>“Since July, pediatric cases of COVID-19 have risen by about 240 percent in the U.S. — underscoring the public health need for vaccination. These trial results provide a strong foundation for seeking authorization of our vaccine for children 5 to 11 years old, and we plan to submit them to the FDA and other regulators with urgency,” said Albert Bourla, the chairman and CEO for Pfizer.\u003c/p>\n\u003cp>“Over the past nine months, hundreds of millions of people ages 12 and older from around the world have received our COVID-19 vaccine. We are eager to extend the protection afforded by the vaccine to this younger population, subject to regulatory authorization, especially as we track the spread of the Delta variant and the substantial threat it poses to children,” Bourla said in a statement.\u003c/p>\n\u003cp>Despite the strong results, it will be some time before the general public can see an official rollout of vaccines for children ages 5 to 11. Once analysis of the trial is completed, Pfizer and BioNTech will submit the results “in the near term” to the Food and Drug Administration for review and possible emergency use authorization.\u003c/p>\n\u003cp>And even if the FDA grants that authorization, Dr. Francis Collins, director of the National Institutes of Health, recently told NPR that parents and caregivers will likely have to wait until the end of 2021 before a COVID-19 vaccine is fully approved for young children ages 5 to 11.\u003c/p>\n\u003cp>Trial results for children under 5 years of age could come later this year, the pharmaceutical companies said.\u003c/p>\n\u003cp>\u003c/p>\n\u003cp>“Already in March 2021, we have started the study to evaluate the immunization of younger children. Our objective was to generate and submit the data for schoolkids to regulatory authorities around the world before the winter season begins,” BioNTech CEO and co-founder Ugur Sahin said.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=COVID+Vaccine+For+Kids+Ages+5+To+11+Is+Safe+And+Effective%2C+Pfizer+Says&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"title": "Why Some FDA Scientists Are Arguing Against COVID Boosters",
"headTitle": "Why Some FDA Scientists Are Arguing Against COVID Boosters | KQED",
"content": "\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">F\u003c/span>\u003c/span>ood and Drug Administration scientists have expressed skepticism about the need for additional doses of Pfizer’s COVID-19 vaccine for all people who have received it.\u003c/p>\n\u003cp>The assessment by the agency’s staff, included in \u003ca href=\"https://www.fda.gov/advisory-committees/advisory-committee-calendar/vaccines-and-related-biological-products-advisory-committee-september-17-2021-meeting-announcement\" target=\"_blank\" rel=\"noopener noreferrer\">documents released Wednesday\u003c/a>, sets up a high-stakes debate over who will need an additional booster dose — and when they will need it — at the meeting of experts being convened by the Food and Drug Administration on Friday.\u003c/p>\n\u003cp>In the documents, the FDA’s own scientists seemed to strike a skeptical position about the need for widespread booster shots. Overall, they said, “data indicate that currently US-licensed or authorized COVID-19 vaccines still afford protection against severe COVID-19 disease and death in the United States.”\u003c/p>\n\u003cp>Other data released Wednesday, both in briefing documents for the Friday panel and by other researchers, add to the swirling debate over a question that will affect millions of people who have been vaccinated against COVID-19 around the world: If the effectiveness of the vaccine wanes, do people need to top it off with an additional dose? If so, when should that happen given that much of the world has not received a first dose of vaccine yet? And should that decision vary by age and by whether people have other health conditions that could make Covid worse if they do become infected with the SARS-CoV-2 virus?\u003c/p>\n\u003cp>On one side are drug companies and some researchers, who point to data showing the efficacy of the vaccines to protect all infections is waning and that a third shot will provide additional protection. On the other are those who point out that these vaccines are still keeping people out of the hospital and preventing them from dying, indicating that a booster is not needed yet.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>The advice of the FDA’s advisory panel on the matter will not be binding, but the agency is likely to consider it. If the FDA authorizes a booster dose, the decision on whether to give them broadly will be taken up by a separate advisory committee convened by the Centers for Disease Control and Prevention. There has been no date set yet for a meeting of that group, the Advisory Committee on Immunization Practices.\u003c/p>\n\u003cp>Still, any decision by the FDA that limits the approval for booster shots, or even expresses hesitancy about how they should be used, will be seen as a rebuke to the Biden administration, which in August took the unusual step of unveiling a plan to offer boosters to the U.S. population, ahead of decisions from the FDA and the CDC.\u003c/p>\n\u003cp>Among those who have challenged the need for boosters at this point are two senior FDA officials who recently announced \u003ca href=\"https://www.statnews.com/2021/08/31/top-vaccine-officials-leave-fda/\" target=\"_blank\" rel=\"noopener noreferrer\">they will retire\u003c/a> from the agency this fall, a move seen to be motivated by their disagreement with the administration on the booster question. Marion Gruber and Phil Krause, director and deputy director, respectively, of FDA’s Office of Vaccines Research and Review, were also co-authors of a \u003ca href=\"https://www.statnews.com/2021/09/13/international-review-argues-against-covid-19-vaccine-boosters/\" target=\"_blank\" rel=\"noopener noreferrer\">paper published Monday\u003c/a> in The Lancet that argued against the need for booster shots for the general public at this time.\u003c/p>\n\u003cp>In the briefing documents made available Wednesday, Pfizer argued that the effectiveness of its vaccine is declining and that a third dose would return efficacy to the 95% level seen in clinical trials.\u003c/p>\n\u003cp>Recent data from Israel showed the efficacy of the vaccine against infection with SARS-CoV-2 dropped from 95% in January to 39% in June. In an analysis of Pfizer’s own Phase 3 trial, which resulted in the vaccine’s approval, the incidence of breakthrough cases was higher among patients who received their second dose before December 2020 than in those who received their second dose after March.\u003c/p>\n\u003cp>The company also released new data from a study conducted by Kaiser Permanente in Southern California that showed the waning efficacy is likely due to the vaccine becoming less effective over time, not because the new Delta variant is more resistant to the vaccine.\u003c/p>\n\u003cp>In the Kaiser data, the efficacy of the vaccine at preventing SARS-CoV-2 infection with the Delta variant dropped from 93% for those vaccinated less than one month to 53% for those vaccinated more than four months ago. For other variants, this drop was from 97% to 67%. At this point, about 88% of SARS-2 viruses detected globally are from the Delta family.\u003c/p>\n\u003cp>However, the vaccine still did a very good job preventing hospitalizations in this dataset, reducing hospitalization by 93% in cases infected with the Delta variant.\u003c/p>\n\u003cp>“It should be recognized that while observational studies can enable understanding of real-world effectiveness, there are known and unknown biases that can affect their reliability,” FDA scientists state in their report. “Due to these biases some studies may be more reliable than others. Furthermore, US-based studies of post- authorization effectiveness of [the vaccine] may most accurately represent vaccine effectiveness in the US population.”\u003c/p>\n\u003cp>The FDA documents assessed questions about the \u003ca href=\"https://www.statnews.com/2021/09/07/how-risk-side-effects-could-change-covid-19-vaccine-boosters/\" target=\"_blank\" rel=\"noopener noreferrer\">safety of giving a third dose of the vaccine\u003c/a>, noting that for some issues, there are no answers. For instance, it is not known if a third dose would trigger elevated rates of myocarditis and pericarditis, a side effect seen mainly in males under the age of 40.\u003c/p>\n\u003cp>“It is currently not known if there will be an increased risk of myocarditis/pericarditis or other adverse reactions after a booster dose of Comirnaty. These risks and associated uncertainties have to be considered when assessing benefit and risk,” the agency’s scientists wrote. Comirnaty is the brand name of Pfizer’s vaccine.\u003c/p>\n\u003cp>Meanwhile, an \u003ca href=\"https://khub.net/documents/135939561/338928724/Vaccine+effectiveness+and+duration+of+protection+of+covid+vaccines+against+mild+and+severe+COVID-19+in+the+UK.pdf/10dcd99c-0441-0403-dfd8-11ba2c6f5801\" target=\"_blank\" rel=\"noopener noreferrer\">analysis of vaccine efficacy from the United Kingdom\u003c/a> — the first country to begin vaccination with the vaccines developed in the West — gives further ammunition to those who have argued that booster shots for all are not warranted at this time.\u003c/p>\n\u003cp>The analysis from Public Health England, which has not yet been peer-reviewed, found protection against hospitalization and deaths remains high for the Pfizer jab, even among older adults who are healthy.\u003c/p>\n\u003cp>“Given the sustained high [vaccine efficacy] against hospitalization and death, the additional benefit of a third dose against these more serious outcomes is limited in the current epidemiological situation,” the authors of the British study concluded. They added that vaccine efficacy “may, however, continue to wane over time and it is likely that booster doses may have a bigger impact on the more severe outcomes with longer intervals between the second and third doses.”\u003c/p>\n\u003cp>The most significant waning of protection is occurring in people aged 65 and older who have significant health issues, the paper said. It is based on a comparison of the vaccination status of nearly 1.5 million people who tested positive for Covid-19 to nearly 3.3 million people who tested negative for the virus.\u003c/p>\n\u003cp>“We found that waning was greatest among individuals in clinical risk groups, suggesting that this group should be prioritized for boosters, whenever they are recommended,” the authors said.\u003c/p>\n\u003cp>Despite the findings, Britain’s Joint Committee on Vaccination and Immunization recommended Wednesday that everyone who was at the front of the line when the country began its vaccine rollout last December should receive a booster shot, once six months had passed since their second jab.\u003c/p>\n\u003cp>Those listed as being at the head of the priority list for boosters in the U.K. are those living in long-term care facilities, adults 50 years of age and older, front-line health care workers and social workers, people 16 to 49 years old with underlying health conditions that put them at high risk of developing severe disease if they contract the virus, and adults who live with immunocompromised people.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003caside class=\"read-more standard\">\u003c/aside>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>\u003cspan class=\"big-cap-wrap\">\u003cspan class=\"big-cap\">F\u003c/span>\u003c/span>ood and Drug Administration scientists have expressed skepticism about the need for additional doses of Pfizer’s COVID-19 vaccine for all people who have received it.\u003c/p>\n\u003cp>The assessment by the agency’s staff, included in \u003ca href=\"https://www.fda.gov/advisory-committees/advisory-committee-calendar/vaccines-and-related-biological-products-advisory-committee-september-17-2021-meeting-announcement\" target=\"_blank\" rel=\"noopener noreferrer\">documents released Wednesday\u003c/a>, sets up a high-stakes debate over who will need an additional booster dose — and when they will need it — at the meeting of experts being convened by the Food and Drug Administration on Friday.\u003c/p>\n\u003cp>In the documents, the FDA’s own scientists seemed to strike a skeptical position about the need for widespread booster shots. Overall, they said, “data indicate that currently US-licensed or authorized COVID-19 vaccines still afford protection against severe COVID-19 disease and death in the United States.”\u003c/p>\n\u003cp>Other data released Wednesday, both in briefing documents for the Friday panel and by other researchers, add to the swirling debate over a question that will affect millions of people who have been vaccinated against COVID-19 around the world: If the effectiveness of the vaccine wanes, do people need to top it off with an additional dose? If so, when should that happen given that much of the world has not received a first dose of vaccine yet? And should that decision vary by age and by whether people have other health conditions that could make Covid worse if they do become infected with the SARS-CoV-2 virus?\u003c/p>\n\u003cp>On one side are drug companies and some researchers, who point to data showing the efficacy of the vaccines to protect all infections is waning and that a third shot will provide additional protection. On the other are those who point out that these vaccines are still keeping people out of the hospital and preventing them from dying, indicating that a booster is not needed yet.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>The advice of the FDA’s advisory panel on the matter will not be binding, but the agency is likely to consider it. If the FDA authorizes a booster dose, the decision on whether to give them broadly will be taken up by a separate advisory committee convened by the Centers for Disease Control and Prevention. There has been no date set yet for a meeting of that group, the Advisory Committee on Immunization Practices.\u003c/p>\n\u003cp>Still, any decision by the FDA that limits the approval for booster shots, or even expresses hesitancy about how they should be used, will be seen as a rebuke to the Biden administration, which in August took the unusual step of unveiling a plan to offer boosters to the U.S. population, ahead of decisions from the FDA and the CDC.\u003c/p>\n\u003cp>Among those who have challenged the need for boosters at this point are two senior FDA officials who recently announced \u003ca href=\"https://www.statnews.com/2021/08/31/top-vaccine-officials-leave-fda/\" target=\"_blank\" rel=\"noopener noreferrer\">they will retire\u003c/a> from the agency this fall, a move seen to be motivated by their disagreement with the administration on the booster question. Marion Gruber and Phil Krause, director and deputy director, respectively, of FDA’s Office of Vaccines Research and Review, were also co-authors of a \u003ca href=\"https://www.statnews.com/2021/09/13/international-review-argues-against-covid-19-vaccine-boosters/\" target=\"_blank\" rel=\"noopener noreferrer\">paper published Monday\u003c/a> in The Lancet that argued against the need for booster shots for the general public at this time.\u003c/p>\n\u003cp>In the briefing documents made available Wednesday, Pfizer argued that the effectiveness of its vaccine is declining and that a third dose would return efficacy to the 95% level seen in clinical trials.\u003c/p>\n\u003cp>Recent data from Israel showed the efficacy of the vaccine against infection with SARS-CoV-2 dropped from 95% in January to 39% in June. In an analysis of Pfizer’s own Phase 3 trial, which resulted in the vaccine’s approval, the incidence of breakthrough cases was higher among patients who received their second dose before December 2020 than in those who received their second dose after March.\u003c/p>\n\u003cp>The company also released new data from a study conducted by Kaiser Permanente in Southern California that showed the waning efficacy is likely due to the vaccine becoming less effective over time, not because the new Delta variant is more resistant to the vaccine.\u003c/p>\n\u003cp>In the Kaiser data, the efficacy of the vaccine at preventing SARS-CoV-2 infection with the Delta variant dropped from 93% for those vaccinated less than one month to 53% for those vaccinated more than four months ago. For other variants, this drop was from 97% to 67%. At this point, about 88% of SARS-2 viruses detected globally are from the Delta family.\u003c/p>\n\u003cp>However, the vaccine still did a very good job preventing hospitalizations in this dataset, reducing hospitalization by 93% in cases infected with the Delta variant.\u003c/p>\n\u003cp>“It should be recognized that while observational studies can enable understanding of real-world effectiveness, there are known and unknown biases that can affect their reliability,” FDA scientists state in their report. “Due to these biases some studies may be more reliable than others. Furthermore, US-based studies of post- authorization effectiveness of [the vaccine] may most accurately represent vaccine effectiveness in the US population.”\u003c/p>\n\u003cp>The FDA documents assessed questions about the \u003ca href=\"https://www.statnews.com/2021/09/07/how-risk-side-effects-could-change-covid-19-vaccine-boosters/\" target=\"_blank\" rel=\"noopener noreferrer\">safety of giving a third dose of the vaccine\u003c/a>, noting that for some issues, there are no answers. For instance, it is not known if a third dose would trigger elevated rates of myocarditis and pericarditis, a side effect seen mainly in males under the age of 40.\u003c/p>\n\u003cp>“It is currently not known if there will be an increased risk of myocarditis/pericarditis or other adverse reactions after a booster dose of Comirnaty. These risks and associated uncertainties have to be considered when assessing benefit and risk,” the agency’s scientists wrote. Comirnaty is the brand name of Pfizer’s vaccine.\u003c/p>\n\u003cp>Meanwhile, an \u003ca href=\"https://khub.net/documents/135939561/338928724/Vaccine+effectiveness+and+duration+of+protection+of+covid+vaccines+against+mild+and+severe+COVID-19+in+the+UK.pdf/10dcd99c-0441-0403-dfd8-11ba2c6f5801\" target=\"_blank\" rel=\"noopener noreferrer\">analysis of vaccine efficacy from the United Kingdom\u003c/a> — the first country to begin vaccination with the vaccines developed in the West — gives further ammunition to those who have argued that booster shots for all are not warranted at this time.\u003c/p>\n\u003cp>The analysis from Public Health England, which has not yet been peer-reviewed, found protection against hospitalization and deaths remains high for the Pfizer jab, even among older adults who are healthy.\u003c/p>\n\u003cp>“Given the sustained high [vaccine efficacy] against hospitalization and death, the additional benefit of a third dose against these more serious outcomes is limited in the current epidemiological situation,” the authors of the British study concluded. They added that vaccine efficacy “may, however, continue to wane over time and it is likely that booster doses may have a bigger impact on the more severe outcomes with longer intervals between the second and third doses.”\u003c/p>\n\u003cp>The most significant waning of protection is occurring in people aged 65 and older who have significant health issues, the paper said. It is based on a comparison of the vaccination status of nearly 1.5 million people who tested positive for Covid-19 to nearly 3.3 million people who tested negative for the virus.\u003c/p>\n\u003cp>“We found that waning was greatest among individuals in clinical risk groups, suggesting that this group should be prioritized for boosters, whenever they are recommended,” the authors said.\u003c/p>\n\u003cp>Despite the findings, Britain’s Joint Committee on Vaccination and Immunization recommended Wednesday that everyone who was at the front of the line when the country began its vaccine rollout last December should receive a booster shot, once six months had passed since their second jab.\u003c/p>\n\u003cp>Those listed as being at the head of the priority list for boosters in the U.K. are those living in long-term care facilities, adults 50 years of age and older, front-line health care workers and social workers, people 16 to 49 years old with underlying health conditions that put them at high risk of developing severe disease if they contract the virus, and adults who live with immunocompromised people.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cem>This story was originally published by \u003ca href=\"https://www.statnews.com/2020/08/10/winter-is-coming-as-flu-season-nears-americas-window-of-opportunity-to-beat-back-covid-19-is-narrowing/\" target=\"_blank\" rel=\"noopener noreferrer\">STAT\u003c/a>, an online publication of Boston Globe Media that covers health, medicine, and scientific discovery.\u003c/em>\u003c/p>\n\u003caside class=\"read-more standard\">\u003c/aside>\n\n\u003c/div>\u003c/p>",
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"content": "\u003cp>Like millions of others, Kathleen Hipps thought she was safe from COVID-19 after she got two shots of the Moderna vaccine last spring. So she figured she just had a summer cold when she got the sniffles in July. But then she opened some Vicks VapoRub.\u003c/p>\n\u003cp>“Anyone who’s ever smelled Vicks VapoRub knows how pungent of a smell it is. And I couldn’t smell it. And that’s how I knew I had COVID,” says Hipps, 40, a Los Angeles lawyer who has two young sons.\u003c/p>\n\u003cp>And sure enough, Hipps tested positive. “I got very sick. I was very tired, very congested — could barely get out of bed. I couldn’t work at all. I had to find colleagues to cover my work for me. And I just spent the next week basically in bed, completely isolated from my family,” she says.\u003c/p>\n\u003cp>Hipps never ran a fever, though, and did not have bad headaches or body aches. She started feeling better after about a week, tested negative and went back to working from home and caring for her family. She thought she was fully recovered.\u003c/p>\n\u003cp>“And I was in my mom’s new car and all of a sudden I felt burning. And I thought there was something wrong with her car,” she says.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>Wherever she moved her foot, she could still feel the burning sensation. And then her other foot started burning, too. It felt like she was walking on hot coals, she says.\u003c/p>\n\u003cp>“I’ve learned that this is neuropathy, and this a common symptom of long COVID,” Hipps says.\u003c/p>\n\u003ch3>Some patients’ symptoms last for weeks or months\u003c/h3>\n\u003cp>\u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects.html\" target=\"_blank\" rel=\"noopener noreferrer\">Long COVID\u003c/a> is a poorly defined, poorly understood condition that occurs when COVID-19 patients’ symptoms won’t go away\u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7992371/\" target=\"_blank\" rel=\"noopener noreferrer\"> for weeks or months,\u003c/a> or new ones emerge just when they think they’re all better.\u003c/p>\n\u003cp>More than six weeks after it started, Hipps still experiences the burning sensation every day, as well as tingling and numbness in her hands.\u003c/p>\n\u003cp>Sometimes the numbness is so bad she can’t push her baby’s stroller. Her periods are really heavy. And work tires her out so fast now that she has to take lots of breaks.\u003c/p>\n\u003cp>“I’m really scared. I mean I’m really scared that there are things that are going on with me that I’m going to have to deal with for the rest of my life,” Hipps says.\u003c/p>\n\u003cp>Now it’s really important to stress that the COVID-19 vaccines are still highly effective at protecting people from getting really sick or dying, and are still quite good at keeping most people from even catching the virus or getting mildly ill.\u003c/p>\n\u003cp>But breakthrough infections can happen, especially with the delta variant. And it’s becoming increasingly clear that unvaccinated people can develop long COVID symptoms, even from mild cases.\u003c/p>\n\u003cp>“We’ve seen that with the infection itself in the unvaccinated individuals about 30% of those individuals continue to have these long-haul COVID symptoms,” says Dr.\u003ca href=\"https://irp.nih.gov/pi/avindra-nath\" target=\"_blank\" rel=\"noopener noreferrer\"> Avindra Nath\u003c/a>, who is studying long COVID at the National Institutes of Health.\u003c/p>\n\u003cp>So the concern is whether vaccinated people who get infected may be at risk for long COVID too, Nath says.\u003c/p>\n\u003cp>“I think that’s a good question,” he says.\u003c/p>\n\u003ch3>Studies look for answers about long COVID\u003c/h3>\n\u003cp>A small\u003ca href=\"https://www.npr.org/transcripts/1021888033\" target=\"_blank\" rel=\"noopener noreferrer\"> Israeli study\u003c/a> recently provided the first evidence that breakthrough infections could lead to long COVID symptoms, although the numbers are small. Out of about 1,500 vaccinated health care workers, 39 got infected, and seven reported symptoms that lasted more than six weeks.\u003c/p>\n\u003cp>And a \u003ca href=\"http://www.thelancet-press.com/embargo/vaxeffectiveness.pdf\">large British study\u003c/a> subsequently found about 5% of people who got infected — even though they were fully vaccinated — experienced persistent symptoms, although the study also found that the odds of having symptoms for 28 days or more were halved by having two vaccine doses.\u003c/p>\n\u003cp>“I think it’s a reasonable concern. But it’s too early. I think we need to follow these patients. It’s quite recent that they’ve been recognized. So at the moment we don’t have that answer,” Nath says, adding that if there is a risk, he suspects it’s probably very low.\u003c/p>\n\u003ch3>But the experts don’t all agree\u003c/h3>\n\u003cp>Some infectious disease experts remain highly skeptical that long COVID from breakthrough infections is a big problem.\u003c/p>\n\u003cp>“Pathophysiologically, it’s quite unlikely to get long COVID from a breakthrough infection,” says Dr.\u003ca href=\"https://profiles.ucsf.edu/monica.gandhi\" target=\"_blank\" rel=\"noopener noreferrer\"> Monica Gandhi\u003c/a>, an infectious disease researcher at UCSF.\u003c/p>\n\u003cp>That’s because the immune response generated by the vaccine would prevent the virus from taking hold in the body or triggering a harmful overreaction by the immune system, Gandhi says.\u003c/p>\n\u003cp>“I think it is absolutely not impossible, but pathophysiologically it is less likely,” she says.\u003c/p>\n\u003cp>Other researchers are convinced the problem is real.\u003c/p>\n\u003cp>“Categorically I can say that we have already seen a handful of cases of long COVID from breakthrough infection,” says\u003ca href=\"https://www.putrinolab.net/\"> David Putrino\u003c/a>, who studies long COVID at Mount Sinai.\u003c/p>\n\u003cp>“We need to behave as though there is the same chance as always of developing long COVID from a mild-to-asymptomatic infection because once you have it you can’t unring that bell and you’re looking at months to years of illness,” Putrino says. Putrino is working with\u003ca href=\"https://medicine.yale.edu/profile/akiko_iwasaki/\"> Akiko Iwasaki\u003c/a>, an immunologist at Yale University, to try to understand how breakthrough infections can lead to persistent symptoms.\u003c/p>\n\u003cp>Iwasaki says some people may experience long COVID because the virus is still hiding in the body. In others, it may be that their immune systems overreact to the virus — a so-called autoimmune response.\u003c/p>\n\u003cp>“We know that the vaccine induces a robust immune response to quickly clear the virus during breakthrough infections,” Iwasaki says. “And that suggests to me that autoimmunity may be the culprit there.”\u003c/p>\n\u003cp>Even if breakthrough infections can lead to long COVID, others say there are also plenty of other reasons vaccinated people should continue to keep being careful to avoid catching the virus.\u003c/p>\n\u003cp>“At the end of the day, my biggest concern honestly is not that I’m going to get long COVID,” says Dr.\u003ca href=\"https://vaccines.emory.edu/faculty-evc/primary-faculty/delrio_carlos.html\" target=\"_blank\" rel=\"noopener noreferrer\"> Carlos del Rio\u003c/a>, an infectious disease researcher at Emory University. “It’s that I’m going to bring COVID and give it to someone else. I mean, I have a young granddaughter. If I get infected, I could give it to her. I’m more concerned that people who are vaccinated can get infected and transmit to others.”\u003c/p>\n\u003cp>For her part, Hipps hopes her symptoms don’t plague her for months or even years.\u003c/p>\n\u003cp>“It’s scary because there’s obviously a lot of things we don’t know about this virus and I’m scared about these long-term implications on my body.”\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>Still, she is glad she got the vaccine. She knows it probably kept her out of the hospital and kept her alive.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=What+We+Know+About+Breakthrough+Infections+And+Long+COVID&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>Like millions of others, Kathleen Hipps thought she was safe from COVID-19 after she got two shots of the Moderna vaccine last spring. So she figured she just had a summer cold when she got the sniffles in July. But then she opened some Vicks VapoRub.\u003c/p>\n\u003cp>“Anyone who’s ever smelled Vicks VapoRub knows how pungent of a smell it is. And I couldn’t smell it. And that’s how I knew I had COVID,” says Hipps, 40, a Los Angeles lawyer who has two young sons.\u003c/p>\n\u003cp>And sure enough, Hipps tested positive. “I got very sick. I was very tired, very congested — could barely get out of bed. I couldn’t work at all. I had to find colleagues to cover my work for me. And I just spent the next week basically in bed, completely isolated from my family,” she says.\u003c/p>\n\u003cp>Hipps never ran a fever, though, and did not have bad headaches or body aches. She started feeling better after about a week, tested negative and went back to working from home and caring for her family. She thought she was fully recovered.\u003c/p>\n\u003cp>“And I was in my mom’s new car and all of a sudden I felt burning. And I thought there was something wrong with her car,” she says.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Wherever she moved her foot, she could still feel the burning sensation. And then her other foot started burning, too. It felt like she was walking on hot coals, she says.\u003c/p>\n\u003cp>“I’ve learned that this is neuropathy, and this a common symptom of long COVID,” Hipps says.\u003c/p>\n\u003ch3>Some patients’ symptoms last for weeks or months\u003c/h3>\n\u003cp>\u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects.html\" target=\"_blank\" rel=\"noopener noreferrer\">Long COVID\u003c/a> is a poorly defined, poorly understood condition that occurs when COVID-19 patients’ symptoms won’t go away\u003ca href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7992371/\" target=\"_blank\" rel=\"noopener noreferrer\"> for weeks or months,\u003c/a> or new ones emerge just when they think they’re all better.\u003c/p>\n\u003cp>More than six weeks after it started, Hipps still experiences the burning sensation every day, as well as tingling and numbness in her hands.\u003c/p>\n\u003cp>Sometimes the numbness is so bad she can’t push her baby’s stroller. Her periods are really heavy. And work tires her out so fast now that she has to take lots of breaks.\u003c/p>\n\u003cp>“I’m really scared. I mean I’m really scared that there are things that are going on with me that I’m going to have to deal with for the rest of my life,” Hipps says.\u003c/p>\n\u003cp>Now it’s really important to stress that the COVID-19 vaccines are still highly effective at protecting people from getting really sick or dying, and are still quite good at keeping most people from even catching the virus or getting mildly ill.\u003c/p>\n\u003cp>But breakthrough infections can happen, especially with the delta variant. And it’s becoming increasingly clear that unvaccinated people can develop long COVID symptoms, even from mild cases.\u003c/p>\n\u003cp>“We’ve seen that with the infection itself in the unvaccinated individuals about 30% of those individuals continue to have these long-haul COVID symptoms,” says Dr.\u003ca href=\"https://irp.nih.gov/pi/avindra-nath\" target=\"_blank\" rel=\"noopener noreferrer\"> Avindra Nath\u003c/a>, who is studying long COVID at the National Institutes of Health.\u003c/p>\n\u003cp>So the concern is whether vaccinated people who get infected may be at risk for long COVID too, Nath says.\u003c/p>\n\u003cp>“I think that’s a good question,” he says.\u003c/p>\n\u003ch3>Studies look for answers about long COVID\u003c/h3>\n\u003cp>A small\u003ca href=\"https://www.npr.org/transcripts/1021888033\" target=\"_blank\" rel=\"noopener noreferrer\"> Israeli study\u003c/a> recently provided the first evidence that breakthrough infections could lead to long COVID symptoms, although the numbers are small. Out of about 1,500 vaccinated health care workers, 39 got infected, and seven reported symptoms that lasted more than six weeks.\u003c/p>\n\u003cp>And a \u003ca href=\"http://www.thelancet-press.com/embargo/vaxeffectiveness.pdf\">large British study\u003c/a> subsequently found about 5% of people who got infected — even though they were fully vaccinated — experienced persistent symptoms, although the study also found that the odds of having symptoms for 28 days or more were halved by having two vaccine doses.\u003c/p>\n\u003cp>“I think it’s a reasonable concern. But it’s too early. I think we need to follow these patients. It’s quite recent that they’ve been recognized. So at the moment we don’t have that answer,” Nath says, adding that if there is a risk, he suspects it’s probably very low.\u003c/p>\n\u003ch3>But the experts don’t all agree\u003c/h3>\n\u003cp>Some infectious disease experts remain highly skeptical that long COVID from breakthrough infections is a big problem.\u003c/p>\n\u003cp>“Pathophysiologically, it’s quite unlikely to get long COVID from a breakthrough infection,” says Dr.\u003ca href=\"https://profiles.ucsf.edu/monica.gandhi\" target=\"_blank\" rel=\"noopener noreferrer\"> Monica Gandhi\u003c/a>, an infectious disease researcher at UCSF.\u003c/p>\n\u003cp>That’s because the immune response generated by the vaccine would prevent the virus from taking hold in the body or triggering a harmful overreaction by the immune system, Gandhi says.\u003c/p>\n\u003cp>“I think it is absolutely not impossible, but pathophysiologically it is less likely,” she says.\u003c/p>\n\u003cp>Other researchers are convinced the problem is real.\u003c/p>\n\u003cp>“Categorically I can say that we have already seen a handful of cases of long COVID from breakthrough infection,” says\u003ca href=\"https://www.putrinolab.net/\"> David Putrino\u003c/a>, who studies long COVID at Mount Sinai.\u003c/p>\n\u003cp>“We need to behave as though there is the same chance as always of developing long COVID from a mild-to-asymptomatic infection because once you have it you can’t unring that bell and you’re looking at months to years of illness,” Putrino says. Putrino is working with\u003ca href=\"https://medicine.yale.edu/profile/akiko_iwasaki/\"> Akiko Iwasaki\u003c/a>, an immunologist at Yale University, to try to understand how breakthrough infections can lead to persistent symptoms.\u003c/p>\n\u003cp>Iwasaki says some people may experience long COVID because the virus is still hiding in the body. In others, it may be that their immune systems overreact to the virus — a so-called autoimmune response.\u003c/p>\n\u003cp>“We know that the vaccine induces a robust immune response to quickly clear the virus during breakthrough infections,” Iwasaki says. “And that suggests to me that autoimmunity may be the culprit there.”\u003c/p>\n\u003cp>Even if breakthrough infections can lead to long COVID, others say there are also plenty of other reasons vaccinated people should continue to keep being careful to avoid catching the virus.\u003c/p>\n\u003cp>“At the end of the day, my biggest concern honestly is not that I’m going to get long COVID,” says Dr.\u003ca href=\"https://vaccines.emory.edu/faculty-evc/primary-faculty/delrio_carlos.html\" target=\"_blank\" rel=\"noopener noreferrer\"> Carlos del Rio\u003c/a>, an infectious disease researcher at Emory University. “It’s that I’m going to bring COVID and give it to someone else. I mean, I have a young granddaughter. If I get infected, I could give it to her. I’m more concerned that people who are vaccinated can get infected and transmit to others.”\u003c/p>\n\u003cp>For her part, Hipps hopes her symptoms don’t plague her for months or even years.\u003c/p>\n\u003cp>“It’s scary because there’s obviously a lot of things we don’t know about this virus and I’m scared about these long-term implications on my body.”\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>Still, she is glad she got the vaccine. She knows it probably kept her out of the hospital and kept her alive.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=What+We+Know+About+Breakthrough+Infections+And+Long+COVID&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"title": "What I Learned From My 'Mild' Breakthrough Case of COVID",
"headTitle": "What I Learned From My ‘Mild’ Breakthrough Case of COVID | KQED",
"content": "\u003cp>The test results that hot day in early August shouldn’t have surprised me — all the symptoms were there. A few days earlier, fatigue had enveloped me like a weighted blanket. I chalked it up to my weekend of travel. Next, a headache clamped down on the back of my skull. Then my eyeballs started to ache. And soon enough, everything tasted like nothing.\u003c/p>\n\u003cp>As a reporter who’s covered the coronavirus since the first confirmed U.S. case landed in Seattle, where I live, I should have known what was coming, but there was some part of me that couldn’t quite believe it. I had a breakthrough case of COVID-19 — despite my two shots of the Pfizer vaccine, the second one in April.\u003c/p>\n\u003cp>I was just one more example of our country’s tug and pull between fantasies of a post-COVID-19 summer and the realities of our still-raging pandemic, where even the vaccinated can get sick.\u003c/p>\n\u003cp>Not only was I sick, but I’d brought the virus home and exposed my 67-year-old father and extended family during my first trip back to the East Coast since the start of the pandemic. It was just the scenario I had tried to avoid for a year and a half. And it definitely was not the summer vacation I had anticipated.\u003c/p>\n\u003cp>Where did I get it? Who knows. Like so many Americans, I had loosened up with wearing masks and social distancing after getting fully vaccinated. We had flown across the country, seen friends, stayed at a hotel, eaten indoors and, yes, even went to a long-delayed wedding with other vaccinated people.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>I ended up in quarantine at my father’s house. \u003ca href=\"https://www.npr.org/2021/09/04/1034281124/more-people-are-relying-on-covid-19-tests-but-experts-say-theyre-not-foolproof\" target=\"_blank\" rel=\"noopener noreferrer\">Two rapid antigen tests \u003c/a>(taken a day apart) came back negative, but I could tell I was starting to feel sick. After my second negative test, the nurse leveled with me. “Don’t hang your hat on this,” she said of the results. Sure enough, a few days later the results of a PCR test for the coronavirus (this one sent to a lab) confirmed what had become obvious by then.\u003c/p>\n\u003cp>It was a miserable five days. My legs and arms ached, my fever crept up to 103 and every few hours of sleep would leave my sheets drenched in sweat. I’d drop into bed exhausted after a quick trip down to the kitchen. To sum it up, I’d put my breakthrough case of COVID-19 right up there with my worst bouts of flu. Even after my fever cleared up, I spent the next few weeks feeling low.\u003c/p>\n\u003cp>Of course, I am very lucky. I didn’t go up against the virus with a naive immune system, like millions of Americans did until vaccines were widely available. And, in much of the world, vaccines are \u003cem>still \u003c/em>a distant promise.\u003c/p>\n\u003cp>“You probably would have gotten much sicker if you had not been vaccinated,” \u003ca href=\"https://providers.ucsd.edu/details/11556/infectious-diseases-hiv/aids\">Francesca Torriani\u003c/a>, an infectious disease physician at the University of California, San Diego, explained to me recently.\u003c/p>\n\u003cp>As I shuffled around my room checking my fever, it was also reassuring to know that my chances of ending up in the hospital were slim, even with the delta variant. And now, about a month later, I’ve made a full recovery.\u003c/p>\n\u003cp>The reality is breakthrough cases are becoming more common. Here’s what you should know about getting a breakthrough case — and what I wish I’d known when those first symptoms laid me low:\u003c/p>\n\u003ch3>Is it time for a reality check about what the vaccines can — and can’t do?\u003c/h3>\n\u003cp>The vaccines aren’t a force field that ward off all things COVID-19. They were given the greenlight because they greatly lower your chance of getting seriously ill or dying.\u003c/p>\n\u003cp>But it was easy for me — and I’m not the only one — to grab onto the idea that, after so many months of trying not to get COVID-19, that the vaccine was, more or less, the finish line. And that made getting sick from the virus unnerving.\u003c/p>\n\u003cp>After all, there were reassuring findings\u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7013e3.htm\"> earlier this year\u003c/a> that the vaccine was remarkably good at stopping any infection, even mild ones. This was a kind of bonus, we were told. And then in May the Centers for Disease Control and Prevention said go ahead and shed your mask if you’re vaccinated.\u003c/p>\n\u003cp>“There was so much initial euphoria about how well these vaccines work,” says \u003ca href=\"https://kingcounty.gov/depts/health/about-us/health-officer.aspx\" target=\"_blank\" rel=\"noopener noreferrer\">Jeff Duchin\u003c/a>, an infectious disease physician and the public health officer for Seattle and King County. “I think we — in the public health community, in the medical community — facilitated the impression that these vaccines are bulletproof.”\u003c/p>\n\u003cp>It’s hard to keep dialing up and down your risk calculations. So if you’d hoped to avoid getting sick at all, even slightly, it may be time for a “reset,” Duchin says. This isn’t to be alarmist but to clear away expectations that COVID-19 is out of your life, and keep up your vigilance about common-sense precautions.\u003c/p>\n\u003cp>With more people vaccinated, the total number of breakthrough infections will rise, and that’s not unexpected, he says. “I don’t think our goal should be to achieve zero risk, because that’s unrealistic.”\u003c/p>\n\u003ch3>How high are my chances of getting a breakthrough case these days?\u003c/h3>\n\u003cp>It used to be quite rare, but the rise of delta has changed the odds.\u003c/p>\n\u003cp>“It’s a totally different ballgame with this delta phase,” says \u003ca href=\"https://www.scripps.edu/faculty/topol/\">Dr. Eric Topol\u003c/a>, a professor of molecular medicine at the Scripps Research Translational Institute in La Jolla, Calif. “I think the chance of having a symptomatic infection has gone up substantially.”\u003c/p>\n\u003cp>But he adds, “Quantifying that in the U.S. is very challenging” because our “data is so shoddy.”\u003c/p>\n\u003cp>The vaccinated still have a considerably lower chance of getting infected than those who aren’t protected that way. Look at data collected from Los Angeles County over the summer as the delta variant started to surge in Southern California: Unvaccinated people were \u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7034e5.htm\">five times more likely to test positive\u003c/a> than those who were vaccinated.\u003c/p>\n\u003cp>Recent research has tried to pin down how well the vaccines are working against preventing any breakthrough cases during the delta surge, but much of that comes from other countries and estimates vary significantly.\u003c/p>\n\u003cp>In the U.S., a study published recently in \u003ca href=\"https://www.nejm.org/doi/full/10.1056/NEJMc2112981\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cem>The New England Journal of Medicine\u003c/em>\u003c/a> concluded that vaccine effectiveness “against any symptomatic disease is considerably lower against the delta variant,” dropping from over 90% earlier in the year before delta was the predominant strain to only about 65% in July. Research on breakthrough infections over the summer in New York found the vaccines were still overall \u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7034e1.htm\" target=\"_blank\" rel=\"noopener noreferrer\">about 80% effective against any infection\u003c/a>. Each study has its limits.\u003c/p>\n\u003cp>It’s hard to disentangle what’s most responsible for the rise in breakthrough infections this summer — whether it’s the delta variant itself, waning immunity in some people or that much of the U.S. dropped public health precautions such as masking.\u003c/p>\n\u003cp>“We don’t have good evidence of what’s the cause, but we do know all of these things coming together are associated with more breakthroughs,” says\u003ca href=\"https://www.hsph.harvard.edu/community-safety/people/rachael-piltch-loeb-phd/\"> Rachael Piltch-Loeb\u003c/a>, a public health researcher at the Harvard T.H. Chan School of Public Health.\u003c/p>\n\u003ch3>How careful do I need to be if I want to avoid a breakthrough?\u003c/h3>\n\u003cp>Looking back, I wish I’d taken some more precautions.\u003c/p>\n\u003cp>And my advice is different now when friends and family tell me they want to avoid having a breakthrough case such as mine: Don’t leave it all up to the vaccine. Wear masks, stay away from big gatherings with unvaccinated people, cut down on travel, at least until things calm down.\u003c/p>\n\u003cp>The U.S. \u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/covid-data/covidview/index.html\">is averaging more than 130,000\u003c/a> coronavirus infections a day (about twice what it was when I fell sick), hospitals are being crushed and the White House has proposed booster shots. Scientists are still making sense of what’s happening with breakthrough cases.\u003c/p>\n\u003cp>What’s clear is that in many parts of the U.S., we’re all more likely to run into the virus than we were in the spring. “Your risk is going to be different if you are in a place that’s very highly vaccinated, with very low level of community spread,” says \u003ca href=\"https://www.uofmhealth.org/profile/922/preeti-n-malani-md\">Preeti Malani\u003c/a>, an infectious disease specialist at the University of Michigan. “The piece that’s important is what’s happening in your community.”\u003c/p>\n\u003cp>Even with delta, the goal is not to go back to a lockdown mindset though, Malani says. “My hope is that people who are fully vaccinated should really feel like this risk is manageable.”\u003c/p>\n\u003cp>She says, “Feel good about spending time with your friends or having a small dinner party, but make sure everyone is vaccinated.”\u003c/p>\n\u003ch3>What does a “mild” case of COVID-19 feel like?\u003c/h3>\n\u003cp>In my case, it was worse than expected, but in the parlance of public health, it was “mild,” meaning I didn’t end up in the hospital or require oxygen.\u003c/p>\n\u003cp>This mild category is essentially a catchall, says \u003ca href=\"https://profiles.ucsf.edu/robert.wachter\" target=\"_blank\" rel=\"noopener noreferrer\">Dr. Bob Wachter\u003c/a>, who chairs the Department of Medicine at the UCSF. “Mild” can be “a day of feeling crummy to being completely laid up in bed for a week, all of your bones hurt and your brain isn’t working well.”\u003c/p>\n\u003cp>“So even if we call them mild cases, as you’ve seen, sometimes these are ones you really don’t want to have if you can avoid it,” he says.\u003c/p>\n\u003cp>There’s not great data on the details of these mild breakthrough infections, but so far it appears that “you do way better than those who are not vaccinated,” says\u003ca href=\"https://healthcare.utah.edu/fad/mddetail.php?physicianID=u1074771&name=sarang-k-yoon\"> Dr. Sarang Yoon\u003c/a>, an occupational medicine specialist at the University of Utah Rocky Mountain Center for Occupational Environmental Health who was part of a nationwide CDC study on breakthrough infections. “In general, in terms of symptom duration, it’s much shorter.”\u003c/p>\n\u003cp>Yoon’s study, published in June with data collected before the delta surge, offers some reassurance: The presence of fever was cut in half, and the days spent in bed reduced by 60% among people with breakthrough infections, compared with unvaccinated people who got sick. “These are meaningful decreases,” says \u003ca href=\"https://medicine.utah.edu/faculty/mddetail.php?facultyID=u0067419\">Matt Thiese\u003c/a>, an epidemiologist and colleague of Yoon’s who worked on the study. “It can be the difference between having a fever for almost nine days and having a fever for just under three days.”\u003c/p>\n\u003cp>A recent study from the U.K. also shows that if you’re sick because of a breakthrough case, it’s generally not as bad, and people have fewer symptoms. In fact, the \u003ca href=\"https://covid.joinzoe.com/post/new-top-5-covid-symptoms\" target=\"_blank\" rel=\"noopener noreferrer\">top five symptoms\u003c/a> for people with a breakthrough infection were headache, sneezing, runny nose, sore throat and loss of smell. Notably absent: fever and persistent cough, which are in the top five for unvaccinated people, according to the data compiled by the U.K. researchers.\u003c/p>\n\u003ch3>If I get a breakthrough infection, how sick could I get?\u003c/h3>\n\u003cp>Even with delta, the chance of getting a case of COVID-19 that’s bad enough to send you to the hospital is still rare.\u003c/p>\n\u003cp>If you’re vaccinated, the\u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7037e2.htm?s_cid=mm7037e2_w\" target=\"_blank\" rel=\"noopener noreferrer\"> risk of being hospitalized is 10 times lower\u003c/a> than if you weren’t vaccinated, according to the latest data from the CDC. Those who get severely and critically ill with a breakthrough case tend to be older — in one study done before delta, \u003ca href=\"https://news.yale.edu/2021/09/07/study-examines-severe-breakthrough-cases-covid-19\">the median age was 80\u003c/a> — with underlying medical conditions such as cardiovascular disease.\u003c/p>\n\u003cp>When I was sick, one thing was in the back of my mind as I monitored my symptoms: Would I have problems catching my breath?\u003c/p>\n\u003cp>Thankfully, when you get exposed, the vaccine has already set you up with antibodies, a first line of defense, that will neutralize parts of the virus that attach to the mucosal surfaces of your upper respiratory tract, says Torriani at UC San Diego.\u003c/p>\n\u003cp>“That initial moment when our body is attacked by the virus, that \u003cem>can\u003c/em> lead to some disease,” she says. It’s a bit of a race.\u003c/p>\n\u003cp>The virus may cause you to get a cold, but, in most people, your immune system will “get its act together and thwart that infection from going down into your lungs,” Wachter says.\u003c/p>\n\u003cp>That later stage of COVID-19 also seems to trigger the immune system to get “overly exuberant” and attack your own body, causing severe respiratory problems such as shortness of breath and destructive inflammation. “So if you can prevent that sort of second stage from happening,” Wachter says, “you can prevent a lot of the severe illness from COVID.” Other parts of your immune system, such as T-cells, are also ready to kick into action if you get sick.\u003c/p>\n\u003cp>If you’re concerned, you can keep an eye on your oxygen levels with a pulse oximeter. That’s much more important than your temperature or symptoms, he says.\u003c/p>\n\u003ch3>Can I spread it to others, and do I need to isolate?\u003c/h3>\n\u003cp>Unfortunately, you still have COVID-19 and need to act like it.\u003c/p>\n\u003cp>Even though my first two tests were negative, I started wearing a mask at my house and keeping my distance from my vaccinated family members. I’m glad I did: No one else got sick.\u003c/p>\n\u003cp>The delta variant is more than two times as contagious as the original strain of the virus and can build up quickly in your upper respiratory tract, as was shown in \u003ca href=\"https://www.npr.org/sections/health-shots/2021/08/06/1025553638/how-a-gay-community-helped-the-cdc-spot-a-covid-outbreak-and-learn-more-about-de\" target=\"_blank\" rel=\"noopener noreferrer\">a cluster of breakthrough infections linked to Provincetown, Mass\u003c/a>., over the summer.\u003c/p>\n\u003cp>“Even in fully vaccinated, asymptomatic individuals, they can have enough virus to transmit it,” says \u003ca href=\"https://www.rockefeller.edu/our-scientists/heads-of-laboratories/952-robert-b-darnell/\">Robert Darnell\u003c/a>, a physician scientist at the Rockefeller University. “Delta is very good at replicating, attaching and inserting itself into cells.”\u003c/p>\n\u003cp>The science isn’t settled about just how likely vaccinated people are to spread the virus, and it does appear that \u003ca href=\"https://www.nature.com/articles/s41591-021-01316-7\" target=\"_blank\" rel=\"noopener noreferrer\">the amount of virus in the nose decreases\u003c/a> faster in people who are vaccinated.\u003c/p>\n\u003cp>Even so, wearing masks and staying isolated from others if you test positive or have symptoms is absolutely critical, Darnell says. He also advises getting tested if you are exposed to someone who has COVID-19, even if you’ve been vaccinated, “because you could very well get infected or ill, and you want to protect those around you, including all the children who aren’t vaccinated.”\u003c/p>\n\u003ch3>Could I get long COVID-19 after a breakthrough infection?\u003c/h3>\n\u003cp>The chance I \u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects.html\">might go on to develop long COVID-19\u003c/a> was front and center in my mind when I had a breakthrough case.\u003c/p>\n\u003cp>While there’s not a lot of data yet, research does show that breakthrough infections can lead to the kind of persistent symptoms that characterize long COVID-19, including brain fog, fatigue and headaches. “Hopefully that number is low. Hopefully it doesn’t last as long and it’s not as severe, but it’s just too early to know these things,” Topol says.\u003c/p>\n\u003cp>Recent research from the U.K. \u003ca href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(21)00460-6/fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">suggests that vaccinated people\u003c/a> are about 50% less likely to develop long COVID-19 than those who are unvaccinated. The underlying cause of long COVID-19 is still not yet known, so it complicates the picture for researchers even more, but this early evidence offers some reassurance.\u003c/p>\n\u003cp>“There may be some symptoms like fatigue [that linger], but studies appear to show that vaccination might also decrease the chances of getting long COVID symptoms,” Torriani says.\u003c/p>\n\u003cp>[ad floatright]\u003c/p>\n\u003cp>This is not true for everyone, and it’s a compelling reason to avoid getting infected altogether, Wachter says. “Some of those mild cases will go on to be long COVID, so you have to factor that in,” he says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=I+Got+A+%27Mild%27+Breakthrough+Case.+Here%27s+What+I+Wish+I%27d+Known&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n",
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"excerpt": "After a year and a half of being COVID-cautious, a fully vaccinated health journalist thought he could finally travel and socialize this summer. The resulting illness didn't feel \"mild\" at all.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The test results that hot day in early August shouldn’t have surprised me — all the symptoms were there. A few days earlier, fatigue had enveloped me like a weighted blanket. I chalked it up to my weekend of travel. Next, a headache clamped down on the back of my skull. Then my eyeballs started to ache. And soon enough, everything tasted like nothing.\u003c/p>\n\u003cp>As a reporter who’s covered the coronavirus since the first confirmed U.S. case landed in Seattle, where I live, I should have known what was coming, but there was some part of me that couldn’t quite believe it. I had a breakthrough case of COVID-19 — despite my two shots of the Pfizer vaccine, the second one in April.\u003c/p>\n\u003cp>I was just one more example of our country’s tug and pull between fantasies of a post-COVID-19 summer and the realities of our still-raging pandemic, where even the vaccinated can get sick.\u003c/p>\n\u003cp>Not only was I sick, but I’d brought the virus home and exposed my 67-year-old father and extended family during my first trip back to the East Coast since the start of the pandemic. It was just the scenario I had tried to avoid for a year and a half. And it definitely was not the summer vacation I had anticipated.\u003c/p>\n\u003cp>Where did I get it? Who knows. Like so many Americans, I had loosened up with wearing masks and social distancing after getting fully vaccinated. We had flown across the country, seen friends, stayed at a hotel, eaten indoors and, yes, even went to a long-delayed wedding with other vaccinated people.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>I ended up in quarantine at my father’s house. \u003ca href=\"https://www.npr.org/2021/09/04/1034281124/more-people-are-relying-on-covid-19-tests-but-experts-say-theyre-not-foolproof\" target=\"_blank\" rel=\"noopener noreferrer\">Two rapid antigen tests \u003c/a>(taken a day apart) came back negative, but I could tell I was starting to feel sick. After my second negative test, the nurse leveled with me. “Don’t hang your hat on this,” she said of the results. Sure enough, a few days later the results of a PCR test for the coronavirus (this one sent to a lab) confirmed what had become obvious by then.\u003c/p>\n\u003cp>It was a miserable five days. My legs and arms ached, my fever crept up to 103 and every few hours of sleep would leave my sheets drenched in sweat. I’d drop into bed exhausted after a quick trip down to the kitchen. To sum it up, I’d put my breakthrough case of COVID-19 right up there with my worst bouts of flu. Even after my fever cleared up, I spent the next few weeks feeling low.\u003c/p>\n\u003cp>Of course, I am very lucky. I didn’t go up against the virus with a naive immune system, like millions of Americans did until vaccines were widely available. And, in much of the world, vaccines are \u003cem>still \u003c/em>a distant promise.\u003c/p>\n\u003cp>“You probably would have gotten much sicker if you had not been vaccinated,” \u003ca href=\"https://providers.ucsd.edu/details/11556/infectious-diseases-hiv/aids\">Francesca Torriani\u003c/a>, an infectious disease physician at the University of California, San Diego, explained to me recently.\u003c/p>\n\u003cp>As I shuffled around my room checking my fever, it was also reassuring to know that my chances of ending up in the hospital were slim, even with the delta variant. And now, about a month later, I’ve made a full recovery.\u003c/p>\n\u003cp>The reality is breakthrough cases are becoming more common. Here’s what you should know about getting a breakthrough case — and what I wish I’d known when those first symptoms laid me low:\u003c/p>\n\u003ch3>Is it time for a reality check about what the vaccines can — and can’t do?\u003c/h3>\n\u003cp>The vaccines aren’t a force field that ward off all things COVID-19. They were given the greenlight because they greatly lower your chance of getting seriously ill or dying.\u003c/p>\n\u003cp>But it was easy for me — and I’m not the only one — to grab onto the idea that, after so many months of trying not to get COVID-19, that the vaccine was, more or less, the finish line. And that made getting sick from the virus unnerving.\u003c/p>\n\u003cp>After all, there were reassuring findings\u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7013e3.htm\"> earlier this year\u003c/a> that the vaccine was remarkably good at stopping any infection, even mild ones. This was a kind of bonus, we were told. And then in May the Centers for Disease Control and Prevention said go ahead and shed your mask if you’re vaccinated.\u003c/p>\n\u003cp>“There was so much initial euphoria about how well these vaccines work,” says \u003ca href=\"https://kingcounty.gov/depts/health/about-us/health-officer.aspx\" target=\"_blank\" rel=\"noopener noreferrer\">Jeff Duchin\u003c/a>, an infectious disease physician and the public health officer for Seattle and King County. “I think we — in the public health community, in the medical community — facilitated the impression that these vaccines are bulletproof.”\u003c/p>\n\u003cp>It’s hard to keep dialing up and down your risk calculations. So if you’d hoped to avoid getting sick at all, even slightly, it may be time for a “reset,” Duchin says. This isn’t to be alarmist but to clear away expectations that COVID-19 is out of your life, and keep up your vigilance about common-sense precautions.\u003c/p>\n\u003cp>With more people vaccinated, the total number of breakthrough infections will rise, and that’s not unexpected, he says. “I don’t think our goal should be to achieve zero risk, because that’s unrealistic.”\u003c/p>\n\u003ch3>How high are my chances of getting a breakthrough case these days?\u003c/h3>\n\u003cp>It used to be quite rare, but the rise of delta has changed the odds.\u003c/p>\n\u003cp>“It’s a totally different ballgame with this delta phase,” says \u003ca href=\"https://www.scripps.edu/faculty/topol/\">Dr. Eric Topol\u003c/a>, a professor of molecular medicine at the Scripps Research Translational Institute in La Jolla, Calif. “I think the chance of having a symptomatic infection has gone up substantially.”\u003c/p>\n\u003cp>But he adds, “Quantifying that in the U.S. is very challenging” because our “data is so shoddy.”\u003c/p>\n\u003cp>The vaccinated still have a considerably lower chance of getting infected than those who aren’t protected that way. Look at data collected from Los Angeles County over the summer as the delta variant started to surge in Southern California: Unvaccinated people were \u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7034e5.htm\">five times more likely to test positive\u003c/a> than those who were vaccinated.\u003c/p>\n\u003cp>Recent research has tried to pin down how well the vaccines are working against preventing any breakthrough cases during the delta surge, but much of that comes from other countries and estimates vary significantly.\u003c/p>\n\u003cp>In the U.S., a study published recently in \u003ca href=\"https://www.nejm.org/doi/full/10.1056/NEJMc2112981\" target=\"_blank\" rel=\"noopener noreferrer\">\u003cem>The New England Journal of Medicine\u003c/em>\u003c/a> concluded that vaccine effectiveness “against any symptomatic disease is considerably lower against the delta variant,” dropping from over 90% earlier in the year before delta was the predominant strain to only about 65% in July. Research on breakthrough infections over the summer in New York found the vaccines were still overall \u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7034e1.htm\" target=\"_blank\" rel=\"noopener noreferrer\">about 80% effective against any infection\u003c/a>. Each study has its limits.\u003c/p>\n\u003cp>It’s hard to disentangle what’s most responsible for the rise in breakthrough infections this summer — whether it’s the delta variant itself, waning immunity in some people or that much of the U.S. dropped public health precautions such as masking.\u003c/p>\n\u003cp>“We don’t have good evidence of what’s the cause, but we do know all of these things coming together are associated with more breakthroughs,” says\u003ca href=\"https://www.hsph.harvard.edu/community-safety/people/rachael-piltch-loeb-phd/\"> Rachael Piltch-Loeb\u003c/a>, a public health researcher at the Harvard T.H. Chan School of Public Health.\u003c/p>\n\u003ch3>How careful do I need to be if I want to avoid a breakthrough?\u003c/h3>\n\u003cp>Looking back, I wish I’d taken some more precautions.\u003c/p>\n\u003cp>And my advice is different now when friends and family tell me they want to avoid having a breakthrough case such as mine: Don’t leave it all up to the vaccine. Wear masks, stay away from big gatherings with unvaccinated people, cut down on travel, at least until things calm down.\u003c/p>\n\u003cp>The U.S. \u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/covid-data/covidview/index.html\">is averaging more than 130,000\u003c/a> coronavirus infections a day (about twice what it was when I fell sick), hospitals are being crushed and the White House has proposed booster shots. Scientists are still making sense of what’s happening with breakthrough cases.\u003c/p>\n\u003cp>What’s clear is that in many parts of the U.S., we’re all more likely to run into the virus than we were in the spring. “Your risk is going to be different if you are in a place that’s very highly vaccinated, with very low level of community spread,” says \u003ca href=\"https://www.uofmhealth.org/profile/922/preeti-n-malani-md\">Preeti Malani\u003c/a>, an infectious disease specialist at the University of Michigan. “The piece that’s important is what’s happening in your community.”\u003c/p>\n\u003cp>Even with delta, the goal is not to go back to a lockdown mindset though, Malani says. “My hope is that people who are fully vaccinated should really feel like this risk is manageable.”\u003c/p>\n\u003cp>She says, “Feel good about spending time with your friends or having a small dinner party, but make sure everyone is vaccinated.”\u003c/p>\n\u003ch3>What does a “mild” case of COVID-19 feel like?\u003c/h3>\n\u003cp>In my case, it was worse than expected, but in the parlance of public health, it was “mild,” meaning I didn’t end up in the hospital or require oxygen.\u003c/p>\n\u003cp>This mild category is essentially a catchall, says \u003ca href=\"https://profiles.ucsf.edu/robert.wachter\" target=\"_blank\" rel=\"noopener noreferrer\">Dr. Bob Wachter\u003c/a>, who chairs the Department of Medicine at the UCSF. “Mild” can be “a day of feeling crummy to being completely laid up in bed for a week, all of your bones hurt and your brain isn’t working well.”\u003c/p>\n\u003cp>“So even if we call them mild cases, as you’ve seen, sometimes these are ones you really don’t want to have if you can avoid it,” he says.\u003c/p>\n\u003cp>There’s not great data on the details of these mild breakthrough infections, but so far it appears that “you do way better than those who are not vaccinated,” says\u003ca href=\"https://healthcare.utah.edu/fad/mddetail.php?physicianID=u1074771&name=sarang-k-yoon\"> Dr. Sarang Yoon\u003c/a>, an occupational medicine specialist at the University of Utah Rocky Mountain Center for Occupational Environmental Health who was part of a nationwide CDC study on breakthrough infections. “In general, in terms of symptom duration, it’s much shorter.”\u003c/p>\n\u003cp>Yoon’s study, published in June with data collected before the delta surge, offers some reassurance: The presence of fever was cut in half, and the days spent in bed reduced by 60% among people with breakthrough infections, compared with unvaccinated people who got sick. “These are meaningful decreases,” says \u003ca href=\"https://medicine.utah.edu/faculty/mddetail.php?facultyID=u0067419\">Matt Thiese\u003c/a>, an epidemiologist and colleague of Yoon’s who worked on the study. “It can be the difference between having a fever for almost nine days and having a fever for just under three days.”\u003c/p>\n\u003cp>A recent study from the U.K. also shows that if you’re sick because of a breakthrough case, it’s generally not as bad, and people have fewer symptoms. In fact, the \u003ca href=\"https://covid.joinzoe.com/post/new-top-5-covid-symptoms\" target=\"_blank\" rel=\"noopener noreferrer\">top five symptoms\u003c/a> for people with a breakthrough infection were headache, sneezing, runny nose, sore throat and loss of smell. Notably absent: fever and persistent cough, which are in the top five for unvaccinated people, according to the data compiled by the U.K. researchers.\u003c/p>\n\u003ch3>If I get a breakthrough infection, how sick could I get?\u003c/h3>\n\u003cp>Even with delta, the chance of getting a case of COVID-19 that’s bad enough to send you to the hospital is still rare.\u003c/p>\n\u003cp>If you’re vaccinated, the\u003ca href=\"https://www.cdc.gov/mmwr/volumes/70/wr/mm7037e2.htm?s_cid=mm7037e2_w\" target=\"_blank\" rel=\"noopener noreferrer\"> risk of being hospitalized is 10 times lower\u003c/a> than if you weren’t vaccinated, according to the latest data from the CDC. Those who get severely and critically ill with a breakthrough case tend to be older — in one study done before delta, \u003ca href=\"https://news.yale.edu/2021/09/07/study-examines-severe-breakthrough-cases-covid-19\">the median age was 80\u003c/a> — with underlying medical conditions such as cardiovascular disease.\u003c/p>\n\u003cp>When I was sick, one thing was in the back of my mind as I monitored my symptoms: Would I have problems catching my breath?\u003c/p>\n\u003cp>Thankfully, when you get exposed, the vaccine has already set you up with antibodies, a first line of defense, that will neutralize parts of the virus that attach to the mucosal surfaces of your upper respiratory tract, says Torriani at UC San Diego.\u003c/p>\n\u003cp>“That initial moment when our body is attacked by the virus, that \u003cem>can\u003c/em> lead to some disease,” she says. It’s a bit of a race.\u003c/p>\n\u003cp>The virus may cause you to get a cold, but, in most people, your immune system will “get its act together and thwart that infection from going down into your lungs,” Wachter says.\u003c/p>\n\u003cp>That later stage of COVID-19 also seems to trigger the immune system to get “overly exuberant” and attack your own body, causing severe respiratory problems such as shortness of breath and destructive inflammation. “So if you can prevent that sort of second stage from happening,” Wachter says, “you can prevent a lot of the severe illness from COVID.” Other parts of your immune system, such as T-cells, are also ready to kick into action if you get sick.\u003c/p>\n\u003cp>If you’re concerned, you can keep an eye on your oxygen levels with a pulse oximeter. That’s much more important than your temperature or symptoms, he says.\u003c/p>\n\u003ch3>Can I spread it to others, and do I need to isolate?\u003c/h3>\n\u003cp>Unfortunately, you still have COVID-19 and need to act like it.\u003c/p>\n\u003cp>Even though my first two tests were negative, I started wearing a mask at my house and keeping my distance from my vaccinated family members. I’m glad I did: No one else got sick.\u003c/p>\n\u003cp>The delta variant is more than two times as contagious as the original strain of the virus and can build up quickly in your upper respiratory tract, as was shown in \u003ca href=\"https://www.npr.org/sections/health-shots/2021/08/06/1025553638/how-a-gay-community-helped-the-cdc-spot-a-covid-outbreak-and-learn-more-about-de\" target=\"_blank\" rel=\"noopener noreferrer\">a cluster of breakthrough infections linked to Provincetown, Mass\u003c/a>., over the summer.\u003c/p>\n\u003cp>“Even in fully vaccinated, asymptomatic individuals, they can have enough virus to transmit it,” says \u003ca href=\"https://www.rockefeller.edu/our-scientists/heads-of-laboratories/952-robert-b-darnell/\">Robert Darnell\u003c/a>, a physician scientist at the Rockefeller University. “Delta is very good at replicating, attaching and inserting itself into cells.”\u003c/p>\n\u003cp>The science isn’t settled about just how likely vaccinated people are to spread the virus, and it does appear that \u003ca href=\"https://www.nature.com/articles/s41591-021-01316-7\" target=\"_blank\" rel=\"noopener noreferrer\">the amount of virus in the nose decreases\u003c/a> faster in people who are vaccinated.\u003c/p>\n\u003cp>Even so, wearing masks and staying isolated from others if you test positive or have symptoms is absolutely critical, Darnell says. He also advises getting tested if you are exposed to someone who has COVID-19, even if you’ve been vaccinated, “because you could very well get infected or ill, and you want to protect those around you, including all the children who aren’t vaccinated.”\u003c/p>\n\u003ch3>Could I get long COVID-19 after a breakthrough infection?\u003c/h3>\n\u003cp>The chance I \u003ca href=\"https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects.html\">might go on to develop long COVID-19\u003c/a> was front and center in my mind when I had a breakthrough case.\u003c/p>\n\u003cp>While there’s not a lot of data yet, research does show that breakthrough infections can lead to the kind of persistent symptoms that characterize long COVID-19, including brain fog, fatigue and headaches. “Hopefully that number is low. Hopefully it doesn’t last as long and it’s not as severe, but it’s just too early to know these things,” Topol says.\u003c/p>\n\u003cp>Recent research from the U.K. \u003ca href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(21)00460-6/fulltext\" target=\"_blank\" rel=\"noopener noreferrer\">suggests that vaccinated people\u003c/a> are about 50% less likely to develop long COVID-19 than those who are unvaccinated. The underlying cause of long COVID-19 is still not yet known, so it complicates the picture for researchers even more, but this early evidence offers some reassurance.\u003c/p>\n\u003cp>“There may be some symptoms like fatigue [that linger], but studies appear to show that vaccination might also decrease the chances of getting long COVID symptoms,” Torriani says.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>This is not true for everyone, and it’s a compelling reason to avoid getting infected altogether, Wachter says. “Some of those mild cases will go on to be long COVID, so you have to factor that in,” he says.\u003c/p>\n\u003cdiv class=\"fullattribution\">Copyright 2021 NPR. To see more, visit https://www.npr.org.\u003cimg decoding=\"async\" src=\"https://www.google-analytics.com/__utm.gif?utmac=UA-5828686-4&utmdt=I+Got+A+%27Mild%27+Breakthrough+Case.+Here%27s+What+I+Wish+I%27d+Known&utme=8(APIKey)9(MDAxOTAwOTE4MDEyMTkxMDAzNjczZDljZA004)\">\u003c/div>\n\n\u003c/div>\u003c/p>",
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"title": "Evaluating the New Mu Variant in California",
"headTitle": "Evaluating the New Mu Variant in California | KQED",
"content": "\u003cp>The delta variant pretty much ruined summer by setting back the pandemic recovery by months. So if the public is feeling wary of any new coronavirus variants, it’s understandable.\u003c/p>\n\u003cp>The latest new strain, called mu, after the Greek letter, is now present in California, with 348 cases having been identified.\u003c/p>\n\u003cp>\u003cstrong>Dr. Peter Chin-Hong\u003c/strong>, an infectious disease specialist at UCSF, joined KQED’s Raquel Maria Dillon this week to discuss this new variant and how much of a risk it is to prolonging the pandemic.\u003c/p>\n\u003cp>The following has been edited for length and clarity.\u003c/p>\n\u003cp>\u003cstrong>Why are epidemiologists watching mu so closely?\u003c/strong>\u003c/p>\n\u003cp>\u003cem>Chin-Hong:\u003c/em> It kind of took over the landscape of viruses in Colombia. In the last month or so, it accounted for up to 40% of cases there and also surrounding countries like Ecuador. And now it may be even higher in Colombia; some estimates are above 90%. Nevertheless, it hasn’t really taken off around the world, making up less than 1% of cases around the world. In fact, in the United States, it’s 0.1-0.2% of the cases sequenced last month.\u003c/p>\n\u003cp>\u003cstrong>When should we start to worry about a new variant?\u003c/strong>\u003c/p>\n\u003cp>I think about three questions that I ask myself every time there’s a new variant. Is it more transmissible? Is it more vaccine-evading or vaccine resistant? And does it make you sicker compared to the regular COVID? Personally, what I look at is tempo. If you remember with delta, it took us by surprise. It was found to be so transmissible in taking over the landscape at a tempo that was breathtaking. In May, it was 5% of cases in California. The next month, it started to go to 25%, then 50%. We are not really seeing that with mu outside of Colombia at this moment.\u003c/p>\n\u003cp>\u003cstrong>What’s your personal assessment of mu? And is it here in the Bay Area?\u003c/strong>\u003c/p>\n\u003cp>Mu is definitely here. It’s in 45 countries and in all of the states in the U.S. It’s here because there’s a lot of travel back and forth between the northern part of South America, where it’s dominant, and California.\u003c/p>\n\u003cp>I’m not dispensing with it; it’s something to watch. I’m also not losing sleep over it. These variants may look scary in the lab. But when they come on to the boxing ring that is life, they all play off against each other. And so far, delta is very, very dominant. It’s bullyish. It’s keeping all these other variants in subjugation.\u003c/p>\n\u003cp>\u003cstrong>Are we going to have to be on guard against new variants forever and ever?\u003c/strong>\u003c/p>\n\u003cp>Yes, unfortunately, until more of us get vaccinated. SARS-CoV-2, the virus itself, isn’t very precise; it’s like it’s using a cheap photocopy machine to make copies of itself. Every time it makes a copy, there’s a little bit of an error in it, like a smudge. And that smudge may confer new superpowers — that’s a new variant being created. Every time it makes a copy, there’s that possibility of mutation. In fact, scientists believe every two weeks there’s a new variant somewhere in the world being created, but only a few rise to the rogues gallery of fame, like delta, like mu, like lamda.\u003c/p>\n\u003cp>[ad fullwidth]\u003c/p>\n\u003cp>\u003cstrong>We’ve heard that viruses generally evolve to be less deadly and more contagious. Is that going to be true with COVID-19?\u003c/strong>\u003c/p>\n\u003cp>The virus has to survive in some way; it doesn’t want to die off completely. So some of these superpowers the variants have are probably going to attenuate. These powers of the new variants have been selected for the variants to be prevalent in the community, but not necessarily to be super lethal and kill off all the hosts. So it gets to the point that we want to probably live with COVID, learn to manage it rather than to fear it.\u003c/p>\n\u003cp>\u003cstrong>Should we jump every time a variant gets an official letter, or should we just chill out?\u003c/strong>\u003c/p>\n\u003cp>I definitely think we have to pay attention to each one of them. I think we have to anticipate, be prepared. It’s exhausting, but we have to be in this state of readiness. It reminds us that we’re living with this virus and we need to engage in conversations with folks who haven’t been vaccinated. Really, vaccination is a powerful ally as we battle mu, iota, delta, lambda, the future variants that don’t even have Greek letters yet.\u003c/p>\n\u003cp>\u003cstrong>I like your superpower metaphor, but what I really want is for the vaccines to grant me superpowers …\u003c/strong>\u003c/p>\n\u003cp>I know, but the vaccines \u003cem>are\u003c/em> giving us superpowers. So I think we just have to believe in them more as a country overall.\u003c/p>\n\u003cp>\u003c/p>\n",
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"excerpt": "The latest new coronavirus strain, called mu, is now present in California, with 348 cases having been identified. Dr. Peter Chin-Hong, an infectious disease specialist at UCSF, discusses how scientists are evaluating this new variant.",
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"description": "The latest new coronavirus strain, called mu, is now present in California, with 348 cases having been identified. Dr. Peter Chin-Hong, an infectious disease specialist at UCSF, discusses how scientists are evaluating this new variant.",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003cp>The delta variant pretty much ruined summer by setting back the pandemic recovery by months. So if the public is feeling wary of any new coronavirus variants, it’s understandable.\u003c/p>\n\u003cp>The latest new strain, called mu, after the Greek letter, is now present in California, with 348 cases having been identified.\u003c/p>\n\u003cp>\u003cstrong>Dr. Peter Chin-Hong\u003c/strong>, an infectious disease specialist at UCSF, joined KQED’s Raquel Maria Dillon this week to discuss this new variant and how much of a risk it is to prolonging the pandemic.\u003c/p>\n\u003cp>The following has been edited for length and clarity.\u003c/p>\n\u003cp>\u003cstrong>Why are epidemiologists watching mu so closely?\u003c/strong>\u003c/p>\n\u003cp>\u003cem>Chin-Hong:\u003c/em> It kind of took over the landscape of viruses in Colombia. In the last month or so, it accounted for up to 40% of cases there and also surrounding countries like Ecuador. And now it may be even higher in Colombia; some estimates are above 90%. Nevertheless, it hasn’t really taken off around the world, making up less than 1% of cases around the world. In fact, in the United States, it’s 0.1-0.2% of the cases sequenced last month.\u003c/p>\n\u003cp>\u003cstrong>When should we start to worry about a new variant?\u003c/strong>\u003c/p>\n\u003cp>I think about three questions that I ask myself every time there’s a new variant. Is it more transmissible? Is it more vaccine-evading or vaccine resistant? And does it make you sicker compared to the regular COVID? Personally, what I look at is tempo. If you remember with delta, it took us by surprise. It was found to be so transmissible in taking over the landscape at a tempo that was breathtaking. In May, it was 5% of cases in California. The next month, it started to go to 25%, then 50%. We are not really seeing that with mu outside of Colombia at this moment.\u003c/p>\n\u003cp>\u003cstrong>What’s your personal assessment of mu? And is it here in the Bay Area?\u003c/strong>\u003c/p>\n\u003cp>Mu is definitely here. It’s in 45 countries and in all of the states in the U.S. It’s here because there’s a lot of travel back and forth between the northern part of South America, where it’s dominant, and California.\u003c/p>\n\u003cp>I’m not dispensing with it; it’s something to watch. I’m also not losing sleep over it. These variants may look scary in the lab. But when they come on to the boxing ring that is life, they all play off against each other. And so far, delta is very, very dominant. It’s bullyish. It’s keeping all these other variants in subjugation.\u003c/p>\n\u003cp>\u003cstrong>Are we going to have to be on guard against new variants forever and ever?\u003c/strong>\u003c/p>\n\u003cp>Yes, unfortunately, until more of us get vaccinated. SARS-CoV-2, the virus itself, isn’t very precise; it’s like it’s using a cheap photocopy machine to make copies of itself. Every time it makes a copy, there’s a little bit of an error in it, like a smudge. And that smudge may confer new superpowers — that’s a new variant being created. Every time it makes a copy, there’s that possibility of mutation. In fact, scientists believe every two weeks there’s a new variant somewhere in the world being created, but only a few rise to the rogues gallery of fame, like delta, like mu, like lamda.\u003c/p>\n\u003cp>\u003c/p>\u003c/div>",
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"content": "\u003cdiv class=\"post-body\">\u003cp>\u003c/p>\n\u003cp>\u003cstrong>We’ve heard that viruses generally evolve to be less deadly and more contagious. Is that going to be true with COVID-19?\u003c/strong>\u003c/p>\n\u003cp>The virus has to survive in some way; it doesn’t want to die off completely. So some of these superpowers the variants have are probably going to attenuate. These powers of the new variants have been selected for the variants to be prevalent in the community, but not necessarily to be super lethal and kill off all the hosts. So it gets to the point that we want to probably live with COVID, learn to manage it rather than to fear it.\u003c/p>\n\u003cp>\u003cstrong>Should we jump every time a variant gets an official letter, or should we just chill out?\u003c/strong>\u003c/p>\n\u003cp>I definitely think we have to pay attention to each one of them. I think we have to anticipate, be prepared. It’s exhausting, but we have to be in this state of readiness. It reminds us that we’re living with this virus and we need to engage in conversations with folks who haven’t been vaccinated. Really, vaccination is a powerful ally as we battle mu, iota, delta, lambda, the future variants that don’t even have Greek letters yet.\u003c/p>\n\u003cp>\u003cstrong>I like your superpower metaphor, but what I really want is for the vaccines to grant me superpowers …\u003c/strong>\u003c/p>\n\u003cp>I know, but the vaccines \u003cem>are\u003c/em> giving us superpowers. So I think we just have to believe in them more as a country overall.\u003c/p>\n\u003cp>\u003c/p>\n\u003c/div>\u003c/p>",
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"tagline": "Where conversation and cultura meet",
"info": "What kind of no sabo word is Hyphenación? For us, it’s about living within a hyphenation. Like being a third-gen Mexican-American from the Texas border now living that Bay Area Chicano life. Like Xorje! Each week we bring together a couple of hyphenated Latinos to talk all about personal life choices: family, careers, relationships, belonging … everything is on the table. ",
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"info": "The Political Mind of Jerry Brown brings listeners the wisdom of the former Governor, Mayor, and presidential candidate. Scott Shafer interviewed Brown for more than 40 hours, covering the former governor's life and half-century in the political game – and Brown has some lessons he'd like to share. ",
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"marketplace": {
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"title": "Marketplace",
"info": "Our flagship program, helmed by Kai Ryssdal, examines what the day in money delivered, through stories, conversations, newsworthy numbers and more. Updated Monday through Friday at about 3:30 p.m. PT.",
"airtime": "MON-FRI 4pm-4:30pm, MON-WED 6:30pm-7pm",
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"info": "The MindShift podcast explores the innovations in education that are shaping how kids learn. Hosts Ki Sung and Katrina Schwartz introduce listeners to educators, researchers, parents and students who are developing effective ways to improve how kids learn. We cover topics like how fed-up administrators are developing surprising tactics to deal with classroom disruptions; how listening to podcasts are helping kids develop reading skills; the consequences of overparenting; and why interdisciplinary learning can engage students on all ends of the traditional achievement spectrum. This podcast is part of the MindShift education site, a division of KQED News. KQED is an NPR/PBS member station based in San Francisco. You can also visit the MindShift website for episodes and supplemental blog posts or tweet us \u003ca href=\"https://twitter.com/MindShiftKQED\">@MindShiftKQED\u003c/a> or visit us at \u003ca href=\"/mindshift\">MindShift.KQED.org\u003c/a>",
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"info": "For decades, the process for how police police themselves has been inconsistent – if not opaque. In some states, like California, these proceedings were completely hidden. After a new police transparency law unsealed scores of internal affairs files, our reporters set out to examine these cases and the shadow world of police discipline. On Our Watch brings listeners into the rooms where officers are questioned and witnesses are interrogated to find out who this system is really protecting. Is it the officers, or the public they've sworn to serve?",
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"info": "Our weekly podcast explores how the media 'sausage' is made, casts an incisive eye on fluctuations in the marketplace of ideas, and examines threats to the freedom of information and expression in America and abroad. For one hour a week, the show tries to lift the veil from the process of \"making media,\" especially news media, because it's through that lens that we see the world and the world sees us",
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"politicalbreakdown": {
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"title": "Political Breakdown",
"tagline": "Politics from a personal perspective",
"info": "Political Breakdown is a new series that explores the political intersection of California and the nation. Each week hosts Scott Shafer and Marisa Lagos are joined with a new special guest to unpack politics -- with personality — and offer an insider’s glimpse at how politics happens.",
"airtime": "THU 6:30pm-7pm",
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"possible": {
"id": "possible",
"title": "Possible",
"info": "Possible is hosted by entrepreneur Reid Hoffman and writer Aria Finger. Together in Possible, Hoffman and Finger lead enlightening discussions about building a brighter collective future. The show features interviews with visionary guests like Trevor Noah, Sam Altman and Janette Sadik-Khan. Possible paints an optimistic portrait of the world we can create through science, policy, business, art and our shared humanity. It asks: What if everything goes right for once? How can we get there? Each episode also includes a short fiction story generated by advanced AI GPT-4, serving as a thought-provoking springboard to speculate how humanity could leverage technology for good.",
"airtime": "SUN 2pm",
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"pri-the-world": {
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"title": "PRI's The World: Latest Edition",
"info": "Each weekday, host Marco Werman and his team of producers bring you the world's most interesting stories in an hour of radio that reminds us just how small our planet really is.",
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"imageSrc": "https://cdn.kqed.org/wp-content/uploads/2024/04/The-World-Podcast-Tile-360x360-1.jpg",
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"radiolab": {
"id": "radiolab",
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"info": "A two-time Peabody Award-winner, Radiolab is an investigation told through sounds and stories, and centered around one big idea. In the Radiolab world, information sounds like music and science and culture collide. Hosted by Jad Abumrad and Robert Krulwich, the show is designed for listeners who demand skepticism, but appreciate wonder. WNYC Studios is the producer of other leading podcasts including Freakonomics Radio, Death, Sex & Money, On the Media and many more.",
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"reveal": {
"id": "reveal",
"title": "Reveal",
"info": "Created by The Center for Investigative Reporting and PRX, Reveal is public radios first one-hour weekly radio show and podcast dedicated to investigative reporting. Credible, fact based and without a partisan agenda, Reveal combines the power and artistry of driveway moment storytelling with data-rich reporting on critically important issues. The result is stories that inform and inspire, arming our listeners with information to right injustices, hold the powerful accountable and improve lives.Reveal is hosted by Al Letson and showcases the award-winning work of CIR and newsrooms large and small across the nation. In a radio and podcast market crowded with choices, Reveal focuses on important and often surprising stories that illuminate the world for our listeners.",
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},
"rightnowish": {
"id": "rightnowish",
"title": "Rightnowish",
"tagline": "Art is where you find it",
"info": "Rightnowish digs into life in the Bay Area right now… ish. Journalist Pendarvis Harshaw takes us to galleries painted on the sides of liquor stores in West Oakland. We'll dance in warehouses in the Bayview, make smoothies with kids in South Berkeley, and listen to classical music in a 1984 Cutlass Supreme in Richmond. Every week, Pen talks to movers and shakers about how the Bay Area shapes what they create, and how they shape the place we call home.",
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},
"science-friday": {
"id": "science-friday",
"title": "Science Friday",
"info": "Science Friday is a weekly science talk show, broadcast live over public radio stations nationwide. Each week, the show focuses on science topics that are in the news and tries to bring an educated, balanced discussion to bear on the scientific issues at hand. Panels of expert guests join host Ira Flatow, a veteran science journalist, to discuss science and to take questions from listeners during the call-in portion of the program.",
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"snap-judgment": {
"id": "snap-judgment",
"title": "Snap Judgment",
"tagline": "Real stories with killer beats",
"info": "The Snap Judgment radio show and podcast mixes real stories with killer beats to produce cinematic, dramatic radio. Snap's musical brand of storytelling dares listeners to see the world through the eyes of another. This is storytelling... with a BEAT!! Snap first aired on public radio stations nationwide in July 2010. Today, Snap Judgment airs on over 450 public radio stations and is brought to the airwaves by KQED & PRX.",
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},
"soldout": {
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