Coronavirus updates March 2023

[missy]

Happy March all


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The virus that won’t quit​

As the pandemic drags us into a fourth year, two key questions are on researchers’ minds: What’s driving the proliferation of immune-evasive variants, and what’s causes the persistent symptoms plaguing some 140 million Covid survivors worldwide? Answers to both have been informed by two different and somewhat unsavory lines of inquiry. In the spring of 2020, when it was widely assumed Covid was purely a respiratory disease, critical care physician Dan Chertow began recruiting participants for a study to find out where the coronavirus goes in the body, how long it stays, and what it does there. Using meticulous analytical methods, he and his colleagues at the National Institutes of Health in Bethesda, Maryland, found the virus traverses the entire body and brain, where it can persist for months. The study, published in the journal Nature in December, raised lots of questions, including whether lingering vestiges of SARS-CoV-2 in patients are causing long Covid symptoms. Chertow’s research was based on autopsies of people who died from Covid and he had no information on any unrelenting symptoms they might have had after catching the virus, so he couldn’t answer that question. But the findings sparked intense efforts by other scientists to locate viral reservoirs in long Covid patients as well as clinical trials to counter prolonged infections with Paxlovid and other antiviral treatments. Meantime, Marc Johnson, a virologist at the University of Missouri, has been studying viral persistence in a different way. He and colleagues have been hunting for unusual coronavirus strains in wastewater and studying the mutants over time to learn what genetic changes help them evade the immune system and what new iterations omicron could throw up next. Johnson’s work has demonstrated that some individuals are shedding SARS-CoV-2 in their fecal waste for a year or more, incubating worrisome immune-evasive variants in their digestive tracts. Finding these chronically infected individuals, learning why the virus is hiding out in their bodies, and finding ways to vanquish the infection might not only stem the emergence of worrisome variants, it could also provide relief for millions of long Covid sufferers. —Jason Gale "

 

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Neutralization of BQ.1, BQ.1.1, and XBB with RBD-Dimer Vaccines​

TO THE EDITOR:​

Figure 1
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Vaccine-Elicited Neutralizing Antibodies against SARS-CoV-2 Variants in Human and Murine Serum Samples.

Several B.1.1.529 (omicron) subvariants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are emerging and have become the dominant strains, such as BF.7, BQ.1, BQ.1.1, and XBB. These variants contain more mutations in the spike protein receptor-binding domain (RBD) than the BA.2 and BA.5 strains (Figure 1A). Therefore, the potential of these omicron subvariants for immune evasion is a concern.
The coronavirus disease 2019 (Covid-19) vaccines with inactivated virus (CoronaVac and BBIBP-CorV) and the ZF2001 protein subunit vaccine1 have been widely used in China and many other countries. In this study, we obtained serum samples from vaccinees (age range, 18 to 59 years) who had received three homologous doses of ZF2001 (the ZF2001 group, 16 participants) or inactivated vaccine (the inactivated-vaccine group, 16 participants) or two doses of inactivated vaccine plus a booster dose of ZF2001 (the heterologous-boost group, 16 participants) (Fig. S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). The neutralizing activities in the serum samples from these participants were analyzed with a panel of pseudoviruses. Details of the study design are provided in the Supplementary Appendix.
In the ZF2001 group, three doses of ZF2001 induced high titers of neutralizing antibodies against the prototype and BA.2 strains (geometric mean titer [GMT], 1302 and 252, respectively), a finding that was consistent with the results of our previous study.2 As compared with the neutralizing GMT of 181 against BA.4 and BA.5 (which have the same spike protein sequence), the neutralizing GMTs against BA.4.6 and BF.7 (which have an additional R346T mutation in the RBD) decreased to 67 and 63, respectively. Seropositivity (defined as a neutralization titer >10 [the limit of detection]) was 44% against BQ.1, 13% against BQ.1.1, and 13% against XBB, and the GMTs were below the limit of detection, indicating immune evasion of these more recent strains (Figure 1B, Figs. S2 and S3, and Table S1).
In the inactivated-vaccine group, the neutralizing GMT was 131 against the prototype isolate, 29 against BA.2, and 26 against BA.4 and BA.5. However, neutralization activities against BA.2.3.20, BA.4.6, BF.7, BQ.1, and BQ.1.1 were at background levels, and no serum sample showed neutralization activity against XBB (Figure 1C).
In the heterologous-boost group, the neutralization profile of the serum samples was similar to that in the ZF2001 group. The neutralizing GMT was 812 against the prototype isolate, 60 against BA.2, 15 against BA.2.3.20, 27 against BA.4 and BA.5, 20 against BA.4.6, and 22 against BF.7. In addition, seropositivity for neutralizing antibodies was 13% against XBB, 13% against BQ.1, and 13% against BQ.1.1 (Figure 1D). These results indicated that BQ.1, BQ.1.1, and XBB showed strong resistance to the vaccine-elicited humoral immunity, a finding that was consistent with the results of another recent analysis.3
Recently, we engineered the homotypic RBD-dimer immunogen4 (which is used in the ZF2001 vaccine) and designed heterotypic chimeric RBD dimers, including prototype–B.1.351 (beta) and B.1.617.2 (delta)–omicron vaccine candidates. They induced relatively broad immune responses against SARS-CoV-2 variants.5 In the current study, we tested their neutralizing activities in murine serum samples. BA.2 RBD homodimer and delta–BA.2 RBD heterodimer were also included as comparators (Figure 1E).
The results showed that XBB and BQ.1.1 strongly escape the antibody responses induced by the prototype RBD homodimer (Figure 1F and Fig. S4). For the BA.2 RBD homodimer, the neutralizing GMTs were more than 105 against BA.1, BA.2, and BA.4 and BA.5; between 104 and 105 against the prototype isolate, beta, delta, BA.2.75, BA.2.3.20, BA.4.6, and BF.7; approximately 103 against BQ.1 and BQ.1.1; and 393 against XBB (Figure 1G). The prototype–beta RBD heterodimer could induce high neutralizing GMTs against the currently circulating BF.7, which probably resulted from the K417N, E484K, and N501Y substitutions in beta RBD (Figure 1H). In comparison, delta–BA.1 and delta–BA.2 RBD heterodimers induced balanced neutralization profiles against the early circulating strains (such as the prototype, beta, and delta) and omicron subvariants (Figure 1I and 1J).
The currently circulating omicron subvariants, especially BQ.1, BQ.1.1, and XBB, showed immune escape to the humoral immunity elicited by prototype strain sequence-based vaccines, such as inactivated vaccine and ZF2001. Our study showed that next-generation and updated Covid-19 vaccines are needed for better protection and pandemic control. Our newly updated delta–omicron BA.1 and BA.2 RBD heterodimers had high neutralizing activities against the emerging omicron subvariants. An analysis of clinical data regarding the delta–omicron BA.1 RBD-dimer vaccine ZF2202 is currently under way (ClinicalTrials.gov number, NCT05616754. opens in new tab).
Dedong Li, M.S.A.
China Agricultural University, Beijing, China
Minrun Duan, B.Eng.
Xiao Wang, B.Sc.
Yunnan University, Kunming, China
Pengyue Gao, B.Sc.
University of Science and Technology of China, Hefei, China
Xin Zhao, Ph.D.
Institute of Microbiology of the Chinese Academy of Sciences, Beijing, China
Kun Xu, Ph.D.
Beijing Institutes of Life Science of the Chinese Academy of Sciences, Beijing, China
[email protected]
George F. Gao, D.Phil.
Institute of Microbiology of the Chinese Academy of Sciences, Beijing, China
Supported by a grant (2020YFA0907100) from the National Key Research and Development Program of China, grants (82202030 and 82222040) from the National Natural Science Foundation of China, and a grant (INV-027420) from the Bill and Melinda Gates Foundation. Dr. Zhao is supported by a grant (20220484181) from the Beijing Nova Program of Science and Technology and a grant (2020092) from the Youth Innovation Promotion Association of the Chinese Academy of Sciences.
Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.
This letter was published on March 1, 2023, at NEJM.org.
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Bivalent Covid-19 Vaccines​

• TO THE EDITOR​

  Citing preliminary immunogenicity results and one study on effectiveness, Offit (Feb. 9 issue)1argues in his Perspective article that the bivalent boosters against SARS-CoV-2 omicron subvariants BA.4 and BA.5 as well as the ancestral strain should not be deployed throughout the entire population. Key available evidence that was omitted by Offit suggests otherwise.
  Davis-Gardner and colleagues, as well as others, found that the bivalent boosters had better immunogenicity against emerging variants, including BQ.1.1 and XBB, than did the monovalent boosters.2 Coronavirus disease 2019 (Covid-19) has taken a tremendous toll on the entire population and resulted in more than 7500 hospitalizations and 1100 deaths in the United States among persons 18 to 49 years of age between September and December 2022 alone, according to the Centers for Disease Control and Prevention. Several studies indicate that the bivalent boosters are clinically effective in reducing the incidences of symptomatic disease, hospitalization, and death across the age spectrum, including among persons 18 to 49 years of age who had been vaccinated previously.3-5 Given the excellent safety profile of the vaccines, which is similar to that of the influenza vaccine among persons 6 months of age or older, the totality of the available evidence supports the vaccination of all currently eligible persons with updated Covid-19 vaccines as an important public health intervention.
  Peter W. Marks, M.D., Ph.D.
  Robert M. Califf, M.D.
  Food and Drug Administration, Silver Spring, MD
  [email protected]
  No potential conflict of interest relevant to this letter was reported.
  This letter was published on March 1, 2023, at NEJM.org.
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Moderna to Make Milestone Payments to NIH for COVID Vaccine​

(Reuters) - Moderna Inc will make certain contingent development, commercial and regulatory milestone payments to the U.S. National Institutes of Health (NIH) related to the development of COVID-19 vaccines, the company said in a filing on Friday.

Moderna and the U.S. government agency had entered into a license agreement in December related to certain patents concerning the COVID vaccine products, the filing showed.

The vaccine maker first disclosed the deal in its fourth-quarter earnings release stating it missed profit estimates hurt by the royalty payment to NIH.

Moderna said under the agreement it would pay low single-digit royalties on future net sales and also minimum annual royalties.


(Reporting by Khushi Mandowara in Bengaluru; Editing by Shailesh Kuber)

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Pfizer/BioNTech Apply for Full FDA Approval of Updated COVID Vaccine​

Pfizer Inc and its German partner BioNTech SE said on Friday they filed an application to the U.S Food and Drug Administration (FDA) for a full approval of their Omicron-adapted COVID-19 vaccine.

The companies are seeking approval of the updated vaccine both as a primary course and a booster dose for individuals 12 years of age and above.

Advisers to the FDA in January had unanimously voted in favor of using the same coronavirus strain for the initial COVID-19 vaccine doses and the boosters to simplify the vaccination regimen in the United States.

If the application is approved, individuals will be able to receive the Omicron-adapted vaccine for their primary dose, rather than using the original vaccine for the primary course before having access to the bivalent vaccine, the company said.


The updated vaccine is currently available in the United States under emergency-use authorization as a single booster dose for people aged 5 years and above, and as the third dose in the three-dose primary series for children 6 months through 4 years of age.





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Untreated COVID Often Involves Relapse, Clarifying Antiviral Rebound Discussion​

Approximately one in four patients with untreated COVID-19 experience symptom relapse, while almost one in three exhibits relapse of viral load, a recent study finds.
These findings offer a natural history of COVID-19 that will inform discussions and research concerning antiviral therapy, lead author Jonathan Z. Li, MD, associate professor of infectious disease at Brigham and Women's Hospital and Harvard Medical School, both in Boston, and colleagues reported in Annals of Internal Medicine.
"There are increasing reports that high-risk patients are avoiding nirmatrelvir-ritonavir due to concerns about post-Paxlovid rebound, but there remains a gap in our knowledge of the frequency of symptom and viral relapse during untreated natural infection," Dr. Li said in a written comment.
To address this gap, Dr. Li and colleagues analyzed data from 563 participants from the placebo group of the Adaptive Platform Treatment Trial for Outpatients with COVID-19 (ACTIV-2/A5401).
From days 0-28, patients recorded severity of 13 symptoms, with scores ranging from absent to severe (absent = 0, mild = 1, moderate = 2, severe = 3). RNA testing was performed on samples from nasal swabs on days 0–14, 21, and 28.
"The symptom rebound definition was determined by consensus of the study team, which comprises more than 10 infectious disease, pulmonary, and critical care physicians, as likely representing a clinically meaningful change in symptoms," Dr. Li said.
Symptom scores needed to increase by at least 4 points to reach the threshold. For instance, a patient would qualify for relapse if they had worsening of four symptoms from mild to moderate, emergence of two new moderate symptoms, or emergence of one new moderate and two new mild symptoms.

The threshold for viral relapse was defined by an increase of at least 0.5 log10 RNA copies/mL from one nasal swab to the next, while high-level viral relapse was defined by an increase of at least 5.0 log10 RNA copies/mL. The former threshold was chosen based on previous analysis of viral rebound after nirmatrelvir treatment in the EPIC-HR phase 3 trial, whereas the high-level relapse point was based on Dr. Li and colleagues' previous work linking this cutoff with the presence of infectious virus.
Their present analysis revealed that 26% of patients had symptom relapse at a median of 11 days after first symptom onset. Viral relapse occurred in 31% of patients, while high-level viral relapse occurred in 13% of participants. In about 9 out 10 cases, these relapses were detected at only one time point, suggesting they were transient. Of note, symptom relapse and high-level viral relapse occurred simultaneously in only 3% of patients.
This lack of correlation was "surprising" and "highlights that recovery from any infection is not always a linear process," Dr. Li said.


Their present analysis revealed that 26% of patients had symptom relapse at a median of 11 days after first symptom onset. Viral relapse occurred in 31% of patients, while high-level viral relapse occurred in 13% of participants. In about 9 out 10 cases, these relapses were detected at only one time point, suggesting they were transient. Of note, symptom relapse and high-level viral relapse occurred simultaneously in only 3% of patients.
This lack of correlation was "surprising" and "highlights that recovery from any infection is not always a linear process," Dr. Li said.
This finding also suggests that untreated patients with recurring symptoms probably pose a low risk of contagion, according to David Wohl, MD, coauthor of the paper and professor of medicine in the division of infectious diseases at the University of North Carolina at Chapel Hill.
Paxlovid may not be to blame for COVID-19 rebound

"These results provide important context for the reports of Paxlovid rebound and show that baseline rates of symptom and viral relapse should be accounted for when studying the risk of rebound after antiviral therapy," Dr. Li said.
Dr. Wohl suggested that these data can also play a role in conversations with patients who experience rebound after taking antiviral therapy.
"Many who have a return of their symptoms after taking Paxlovid blame the drug, and that may be justified, but this study suggests it happens in untreated people too," Dr. Wohl said in a written comment.
Longer antiviral therapy deserves investigation

This is a "very important study" because it offers a baseline for comparing the natural history of COVID-19 with clinical course after antiviral therapy, said Timothy Henrich, MD, associate professor in the division of experimental medicine at University of California, San Francisco.
"Unlike this natural history, where it's kind of sputtering up and down as it goes down, [after antiviral therapy,] it goes away for several days, and then it comes back up; and when it comes up, people have symptoms again," Dr. Henrich said in an interview.
This suggests that each type of rebound is a unique phenomenon and, from a clinical perspective, that antiviral therapy may need to be extended.
"We treat for too short a period of time," Dr. Henrich said. "We're able to suppress [SARS-CoV-2] to the point where we're not detecting it in the nasal pharynx, but it's clearly still there. And it's clearly still in a place that can replicate without the drug."
That said, treating for longer may not be a sure-fire solution, especially if antiviral therapy is started early in the clinical course, as this could delay SARS-CoV-2-specific immune responses that are necessary for resolution, Dr. Henrich added,
"We need further study of longer-term therapies," he said.
An array of research questions need to be addressed, according to Aditya Shah, MBBS, an infectious disease specialist at Mayo Clinic, Rochester, Minn. In a written comment, he probed the significance of rebound in various clinical scenarios.
"What [type of] rebound matters and what doesn't?" Dr. Shah asked. "Does symptom rebound matter? How many untreated and treated 'symptom rebounders' need additional treatment or health care? If rebound does not really matter, but if Paxlovid helps in certain unvaccinated and high-risk patients, then does rebound matter? Future research should also focus on Paxlovid utility in vaccinated but high-risk patients. Is it as beneficial in them as it is in unvaccinated high-risk patients?"
While potentially regimen-altering questions like these remain unanswered, Dr. Henrich advised providers to keep patients focused on what we do know about the benefits of antiviral therapy given the current 5-day course, which is that it reduces the risk of severe disease and hospitalization.
The investigators disclosed relationships with Merck, Gilead, ViiV, and others. Dr. Henrich disclosed grant support from Merck and a consulting role with Roche. Dr. Shah disclosed no conflicts of interest.
This article originally appeared on MDedge.com, part of the Medscape Professional Network.


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Scientists find human antibodies that can block multiple coronaviruses including SARS-CoV-2
Published March 1, 2023 | Originally published on MedicalXpress Breaking News-and-Events


A team of scientists from Scripps Research and the University of North Carolina (UNC) has found antibodies in the blood of certain COVID-19 donors that can block infection from a broad set of coronaviruses—specifically, in people who have recovered from the virus and were then vaccinated. They found this includes not only the COVID-19-causing SARS-CoV-2, but also SARS-CoV-1 and MERS-CoV.

The scientists' detailed study of the antibodies and their virus binding sites, reported on February 15, 2023, in the journal Immunity, could lead to the development of a broad coronavirus vaccine and related antibody therapeutics. Both could be used against future coronavirus pandemics as well as any future variants of SARS-CoV-2.

"We show here that there are individual human monoclonal antibodies that can be found that protect against all three recent deadly coronaviruses: SARS-CoV-1, SARS-CoV-2 and MERS-CoV," says study co-senior author Raiees Andrabi, Ph.D., institute investigator in the Department of Immunology and Microbiology at Scripps Research.

The other Scripps Research co-senior authors were Dennis Burton, Ph.D., professor and James and Jessie Minor Chair of the Department of Immunology and Microbiology, and Ian Wilson, Ph.D., Hansen Professor of Structural Biology and chair of the Department of Integrative Structural and Computational Biology. The co-senior authors from UNC were professor Ralph Baric, Ph.D., and assistant professor Lisa Gralinski, Ph.D.

SARS-CoV-2, along with SARS-CoV-1 (the cause of the 2002-04 SARS outbreak) and MERS-CoV (the cause of deadly Middle East Respiratory Syndrome), belong to a broad grouping of coronaviruses known as betacoronaviruses. These viruses mutate at a modestly high rate, creating a significant challenge for the development of vaccines and antibody therapies against them. Thus, in the case of SARS-CoV-2, although existing vaccines have been very helpful in limiting the toll of disease and death from the pandemic, new SARS-CoV-2 variants have emerged that can spread even among vaccine recipients.

Over the past two years, however, the Andrabi/Burton and Wilson laboratories have been finding evidence that SARS-CoV-2 and other betacoronaviruses have a vulnerable site that does not mutate much. This site, which is in the S2 region (or base) of the viral spike protein, is relatively conserved on betacoronaviruses that infect a variety of animal species. By contrast, current SARS-CoV-2 vaccines mainly target the viral spike protein's relatively mutable S1 region, with which the virus binds to host-cell receptors.

The S2 site plays a key role in how betacoronaviruses progress from receptor-binding to the membrane fusion that enables entry into host cells in the respiratory tract. In a study reported last year, the Andrabi/Burton and Wilson laboratories found that some human antibodies can bind to this site on SARS-CoV-2 in a way that apparently disrupts viral fusion and blocks infection. The existence of such a vulnerable site raises the possibility of targeting it to provide both long-lasting and broad protection against betacoronaviruses. Therefore, the researchers, for the new study, made a more comprehensive search for anti-S2 antibodies in blood samples from human volunteers.

These volunteers were individuals who had recovered from COVID-19, had been vaccinated, or had recovered from COVID-19 and then had been vaccinated. Somewhat to the researchers' surprise, they found that antibodies to the vulnerable S2 site were present in the vast majority of volunteers in the latter group—people who had recovered from COVID-19 and then had been vaccinated—but at a much lower frequency in the others. Overall, the researchers identified and characterized 32 of these S2-targeting antibodies.

In lab virus neutralization studies and in virus-challenge studies with mice at UNC, the researchers found that several of these antibodies provide protection of unprecedented breadth— not only against SARS-CoV-2 but also SARS-CoV-1 and MERS-CoV betacoronaviruses.

"In principle, a vaccination strategy that can induce such antibodies is likely to provide broad protection against a diverse spectrum of betacoronaviruses," says Burton.

Structural studies of several of the antibodies when bound to S2 illuminated their common binding sites and modes of binding, providing key information that should aid the development of future vaccines targeting this region.

"Targeted rational vaccine strategies could take advantage of this molecular information of the interactions of these antibodies with the S2 domain to inform the design of pan-betacoronavirus vaccines" says Wilson.

Indeed, the researchers have already applied their findings to the initial design and testing of a potential "pan-betacoronavirus" vaccine candidate, which if successful could be stockpiled to limit future pandemics. The investigators also envision a therapeutic mix of different S2-targeting antibodies, perhaps as a cocktail with antibodies to other spike regions, that could be taken to prevent infection by a novel betacoronavirus or to reduce disease in those already infected.

This article was originally published on MedicalXpress Breaking News-and-Events.


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[flowing_serenity]

Thank you for your very kind continued updates about these things! They’re very informative and helpful. Much appreciated

 

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35 years of US investment in research led to development of mRNA COVID vaccines
Mary Van Beusekom, MS March 2, 2023
COVID-19

In the three decades leading up to the pandemic, the US government invested $31.9 billion in research that supported the development of mRNA COVID-19 vaccines in 2020, $337 million of which was invested before the pandemic, finds a Brigham and Women's–led study published yesterday in The BMJ.

The researchers searched public databases for government-funded grants on four foundational innovations that directly led to the development of mRNA COVID-19 vaccines, including lipid nanoparticle, mRNA synthesis or modification, spike protein structure, and mRNA vaccine biotechnology from January 1985 to March 2022.

Effort involved 34 NIH research grants
The team identified 34 research grants funded by the National Institutes of Health (NIH) that were directly related to the development of mRNA COVID-19 vaccines in 2020. In combination with other government grants and contracts, the research totaled $31.9 billion.

Of the $337 million invested before the pandemic, NIH invested $116 million (35%) in basic and translational science related to mRNA vaccine technology, while the Biomedical Advanced Research and Development Authority (BARDA) invested $148 million (44%), and the Department of Defense invested $72 million (21%).

After the pandemic began, $29.2 billion (92%) of US public funds went toward buying 2 billion advance vaccine doses, $2.3 billion (7%) was spent on clinical trials, and $108 million (less than 1%) was directed to manufacturing and basic and translational science.

Overall, the government paid $18.1 billion to Moderna ($16.2 billion [89%] for vaccines) and $13.1 million to Pfizer/BioNTech (mostly for vaccines). One billion doses were set aside for international donation from Pfizer at a much lower price than those for Americans.

"Although the public funding supporting Moderna is widely recognized, Pfizer-BioNTech executives have claimed that the company did not accept any US government support to develop its vaccine," the authors wrote. "However, Pfizer-BioNTech would not have been able to develop an mRNA covid-19 vaccine without the licensed technologies emerging from research funded by US taxpayers."

The researchers noted the study likely underestimates the true prepandemic public investment, because it didn't include those from other countries, foundations, or companies.

Pfizer-BioNTech would not have been able to develop an mRNA covid-19 vaccine without the licensed technologies emerging from research funded by US taxpayers.
"The development of mRNA COVID-19 vaccines during the pandemic was a monumental scientific success and was possible because of the scientific discoveries that took place in the preceding decades," corresponding author Hussain Lalani, MD, MPH, of Brigham and Women's Hospital, said in a Brigham news release.

But the authors called for policy reforms and follow-up on technology licenses to ensure that manufacturers are making the vaccines appropriately available to equitably support global public health. "mRNA vaccines have saved millions of lives," Lalani said. "The substantial public investment in research that led to these vaccines should justify equitable and affordable access to these lifesaving vaccines globally."

Public risk, private rewards
In a commentary in the same journal, Victor Roy, MD, PhD, of the Yale School of Medicine, said that while mRNA COVID-19 vaccines are a significant achievement, their development illustrates how society invested in and bore the risk of pursuing such innovation while corporate shareholders reaped most of the rewards.

Fueled largely by the global sale of their COVID-19 vaccines, Moderna and Pfizer have made more than $100 billion in global revenues, which Roy pointed out is more than 20 times the World Health Organization's budget for 2020-21.

"Yet for a vaccine that is estimated to cost $1-3 per dose to manufacture, both Moderna and Pfizer have announced plans to charge more than $110 a dose in the US this year—a price that Moderna’s CEO Stephan Bancel has argued is 'consistent with the value' of these vaccines," he wrote.

Yet for a vaccine that is estimated to cost $1-3 per dose to manufacture, both Moderna and Pfizer have announced plans to charge more than $110 a dose in the US this year.
Victor Roy, MD, PhD

To better direct the value it helped create, Roy argued, the US government should have pursued a goal of global COVID-19 vaccination by guiding decisions about intellectual property and technology transfer.

"Secondly, to achieve public goals, the US government can use its position as a pivotal investor and buyer to set conditions in contracts," he said. "These conditions would relate to pricing and access, technology transfer, and reinvestment in innovation."

Last, Roy said governments should build public investment options to make important health technologies, which would secure supplies during public health crises, allow reinvestment of revenues into domestic innovation and manufacturing, and offer negotiating leverage for fairer agreements with private manufacturers.

"Instead of maximizing value for corporate shareholders, these alternatives would enable governments to translate public investments more fully in the service of public health—a fundamental priority as we examine our response to this pandemic and prepare for the next," he concluded.

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[missy]

Thank you for your very kind continued updates about these things! They’re very informative and helpful. Much appreciated

Thank you

 

[missy]

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COVID-19: Bacterial co-infection is a major risk factor for death, ICU admission and mechanical ventilation
Published March 1, 2023 | Originally published on MedicalXpress Breaking News-and-Events

Bacterial co-infection is a major risk factor for death, intensive care unit admission and mechanical ventilation, according to a multi-center, retrospective cohort study published in the journal Critical Care and led by University of Alabama at Birmingham researchers.

Coronavirus disease 2019, or COVID-19, has killed more than 6.3 million people worldwide.

This recent study of 13,781 COVID-19 inpatient encounters from 2020 to 2022 found that bacterial co-infection in the blood, known as bacteremia, is a greater risk factor for death, intensive care unit admission and mechanical ventilation than previously described risk factors for COVID-19 severity and mortality, such as advanced age, male sex or various comorbidities.

The study reviewed COVID-19 inpatient encounters at UAB Hospital and at Ochsner Louisiana State University Health Shreveport hospitals and divided them into three groups: confirmed bacterial co-infection, as measured by a blood test at 48 hours after admission; suspected bacterial co-infection in patients receiving antimicrobials; and no bacterial co-infection.

Bacterial co-infection is a known major source of sickness and death in the context of other respiratory viral infections such as influenza, parainfluenza or RSV. However, it has been unclear regarding the frequency of bacteremic co-infection in COVID-19 and the impact it has on clinical outcomes.

"Although confirmed bacteremic co-infections are rare in COVID-19, less than 4 percent of inpatient admissions, our results show that COVID-19 patients with these co-infections have a staggering 25 percent risk of death at 30 days in UAB patients and a similar risk of 20 percent at Ochsner Louisiana State University Health Shreveport, or OLHS," said Amit Gaggar, M.D., Ph.D., UAB Department of Medicine Division of Pulmonary, Allergy and Critical Care Medicine. Gaggar, in collaboration with the Hugh Kaul Precision Medicine Institute director, Matthew Might, Ph.D., and infectious disease physician-scientist Nathaniel Erdmann, M.D., Ph.D., co-led the study.

"These results strongly suggest an underappreciated interaction between bacterial pathogens and the COVID-19 virus, SARS-CoV-2, and their impact on clinical outcomes," co-senior author Erdmann added.

Specifically, the researchers found that the in-hospital mortality for COVID-19 co-infections of 26 percent at UAB and 22 percent at OLHS exceeded that of the suspected co-infection (UAB, 24 percent; OLHS, 12 percent) and the no co-infection groups (UAB, 5.9 percent; OLHS, 5.1 percent). Furthermore, a control group of 1,703 UAB inpatients with community-acquired bacteremia during a period before the COVID-19 pandemic had a 5.9 percent in-hospital mortality rate.

The researchers also identified laboratory trends associated with COVID-19 bacterial co-infection—a neutrophil-to-lymphocyte ratio of 15 or greater, and the Systemic Inflammatory Response Syndrome, or SIRS, criteria of abnormal white blood cell counts or a heart rate greater than 90 beats per minute. These can help health care providers discriminate COVID-19 bacterial co-infections within 24 hours of admission.

"These results emphasize the role of bacteria in SARS-CoV-2 mortality, and highlight the potential for neutrophil-to-lymphocyte ratio as a rapid and easily available prognostic biomarker of bacterial coinfection and, relatedly, disease severity," said co-senior author Might.

Strengths of this study were the two large, demographically diverse, independent cohorts—UAB reflects an academic hospital and Level I trauma center serving five surrounding states, and OLHS includes encounters from rural, suburban and academic medical centers across the state of Louisiana. Both cohorts overall were well matched for patient age, race, sex and inpatient length of stay.

"One of the novel opportunities of the COVID-19 pandemic has been the seismic shift in collected and searchable data captured by electronic medical record, or EMR, systems. This resource, in combination with the collaborative spirit of experts from UAB and OLHS, provides the bedrock for biomedical informatic studies that can produce clinically useful observations for the betterment of patients," said primary and corresponding author of the study Michael John Patton, an aspiring clinician and biomedical informatician in UAB's Medical Scientist Training Program for M.D.-Ph.D. trainees.

This article was originally published on MedicalXpress Breaking News-and-Events.

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84% of hospital COVID patients in Sweden still had symptoms at 2 years​

Mary Van Beusekom, MS

The vast majority—84.2%—of COVID-19 survivors in a Swedish cohort reported persistent symptoms affecting daily life 2 years after hospital release, according to a follow-up study published late last week in The Lancet Regional Health Europe.

Linkoping University researchers in Sweden interviewed COVID-19 patients about 37 symptoms 2 years after release from the hospital from Mar 1 to May 31, 2020. The group's initial 2021 study found that 185 of 433 hospital patients (42.7%) had lingering symptoms and activity limitations 4 months after discharge.

Of the 181 long-COVID patients still alive at 2 years, 165 agreed to participate in the follow-up study, 63.0% were men, and 26% had been admitted to an intensive care unit (ICU). Of the 47 ICU patients, the median hospital stay was 25 days, and 43 (91%) had received mechanical ventilation for a median of 17 days. Median length of stay among nonseverely ill patients was 4 days.

Fewer patients employed, in classes
During the 2-year study period, 21.2% of the 165 patients were rehospitalized for cardiovascular, trauma/injuries, urogenital and endocrine diseases, infectious diseases such as COVID-19 reinfections, and other conditions. Fully 84.2% said they still had symptoms that had at least moderate effects on their daily life.

At 2 years, 19.4% of patients required referral to a medical clinic for additional follow-up. Cognitive and sensorimotor symptoms and fatigue were the most common lingering symptoms, while there was significant improvement in sensorimotor deficits, affective symptoms, and mental fatigue.

About half of long-COVID patients who were on sick leave at 4 months were still on sick leave at 2 years. The number of patients who were employed or studying was significantly lower at 2 years than before COVID-19.

There was no difference in symptoms between who were or weren't critically ill during initial infection. The number of asymptomatic patients rose from 14 (8%) at 4 months to 41 (25%) at 2 years.

The number of patients who were employed or studying was significantly lower at 2 years than before COVID-19.
The rate of symptoms with at least a moderate impact on daily activities fell significantly by 2 years for limb weakness/fatigability, problems walking at least 1 kilometer (0.6 mile), challenges being physically active, difficulty managing work and/or studies, increased need for sleep, headache, mental fatigue, and anxiety.

Thirty-one patients (18.8%) reported other symptoms not included in the interview, such as heart palpitations, chronic fever, reduced appetite, sweating, and hair loss.

Vaccinated report better health
The degree of shortness of breath improved significantly from 4 months to 2 years, although the proportion of patients with light or moderate shortness of breath was comparable at both assessments (60% and 58%, respectively), and the proportion of severe shortness of breath declined from 32% to 18%.

Self-reported general health improved over the study period, with the number describing their health as good or very good climbing from 35 (22%) to 80 (49%). In a subgroup analysis, the 10 unvaccinated patients said their health had deteriorated over the study period, while the 122 patients who had received at least three vaccine doses patients said their health had improved.

"Our cohort of patients, who were hospitalised with COVID-19 during the first pandemic wave and showed symptoms indicating PCC [post-COVID condition] at 4-months post-discharge, showed improved symptoms at two years post-admission, but also a high prevalence of persistent cognitive, sensorimotor and fatigue symptoms impacting on their everyday life," the researchers wrote. "This implies a need to establish routines for long-term follow-up of patients previously hospitalised due to COVID-19 with PCC."

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CIDRAP unveils roadmap for advancing better coronavirus vaccines​

Lisa Schnirring

Before the COVID-19 pandemic, the warning signs for newly emerging and deadly coronaviruses were already flashing bright red. Researchers were still working on SARS-CoV studies in 2012 when the even deadlier MERS-CoV arrived on the scene in the Middle East, repeatedly jumping from camels over the years and sparking large healthcare-related outbreaks.

As scientists track the rapidly changing SARS-CoV-2 evolution, others are testing and sequencing animal samples to sift out the ones that might pose the next threat to humans. Taken together, the developments have led to a stark realization: The vaccines that worked so well to cut severe illness and death during COVID-19 aren't enough to protect people from the current virus, which has become a moving target, or the novel coronaviruses that will certainly follow.

To help jump-start the search for better vaccines, the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota today released the Coronavirus Vaccines Research and Development (R&D) Roadmap (CVR), a strategy to develop broadly protective vaccines—suitable for use in all world regions—to tackle both threats. Armed with $1 million in support from The Rockefeller Foundation and the Bill & Melinda Gates Foundation, CIDRAP pulled together an international collaboration of 50 scientists who mapped out a strategy to make the new vaccines a reality.

Michael Osterholm, PhD, MPH, CIDRAP's director and professor at the University of Minnesota, said COVID-19 taught the world a hard lesson, that it must be better prepared, and rather than waiting for a fourth coronavirus to emerge or the arrival of a dangerous SARS-CoV-2 subvariant, the time to act is now. "If we wait for the next event to happen before we act, it will be too late."

Research scientist
gorodenkoff / iStock
CIDRAP publishes CIDRAP News, but its news service operates independently of its research and policy efforts.

A heavy lift by a driven scientific team
Bruce Gellin, MD, MPH, a CVR steering group member and chief of public health strategy at The Rockefeller Foundation, said there's an urgency to carve out what to do next. He said the push for a more broadly protective vaccine needs to be some sort of equivalent to Operation Warp Speed (OWS), a public-private partnership that accelerated the development, production, and distribution of COVID-19 vaccines in the United States.

He emphasized that an approach like OWS shows what can happen when people put their mind to it with a process that's a lot of work, but done in a metered way.

If we wait for the next event to happen before we act, it will be too late.
CIDRAP Director Michael Osterholm, PhD, MPH

The key goal is to protect people when they need it, Gellin said. Alongside making the case for urgency, the CVR clearly describes the next steps, with each goal supported by milestones and dates—details that are also useful for policymakers and funders, he added.

The grant was announced last April, and by October the group had already released a draft version for public review and comment. Osterholm said the CVR approach draws on a similar roadmap strategy CIDRAP has used for other projects, including a recent game plan for improving seasonal flu vaccines and developing a universal influenza vaccine.

For the CVR, the path has been complicated by a maze of scientific questions that still need to be answered and by the fact that scientists and policymakers who helped with the CVR are still grappling with the demands of the pandemic itself.

Osterholm said the CVR group was blessed by the level of support from the research community. "We literally had people working at all hours of the day—this was a heavy lift," he said. "We had to summarize work that had never been summarized before."

Five key topics, from bat sampling to investments
The CVR crystalizes key barriers and gaps and lays out specific steps for advancing broadly protective coronavirus vaccines. The team organized its work into five topic areas: virology, immunology, vaccinology, animal and human models for vaccine research, and policy and funding. The full 92-page report is available on CIDRAP's website, and a summary version of it was published today in Vaccine.

In a related commentary in the same issue of Vaccine, Margaret (Peggy) Hamburg, MD, former Food and Drug Administration (FDA) commissioner who serves as chair of the NTI / bio Advisory Group, and Greg Poland, MD, CVR task force member and director of the Mayo Clinic's Vaccine Research Group, wrote that the first-generation COVID-19 vaccines are safe and have done a remarkable job at preventing serious disease. There are down sides, however, including notable reactogenicity for some, short duration of protection, and technical requirements that make them difficult to deploy to remote or low-resource settings.

Hamburg and Poland said the strategy of chasing the latest subvariant and offering frequent booster shots isn't sustainable. "Next-generation vaccines may offer additional benefits such as new methods of delivery—transdermal patches, oral or intranasal vaccines—which are easy to distribute and apply, stimulate mucosal immunity, and potentially block transmission," they wrote.

The two lauded the work that public health groups, manufacturers, and scientists are already doing to advance new vaccines, but they noted that the information is typically siloed. "The CVR recognizes and capitalizes on building bridges between these various sectors and is aimed at reducing barriers and duplication and improving efficiencies," they wrote.

Next-generation vaccines may offer additional benefits such as new methods of delivery—transdermal patches, oral or intranasal vaccines—which are easy to distribute and apply, stimulate mucosal immunity, and potentially block transmission.
Margaret Hamburg, MD, and Greg Poland, MD

Failure to act now puts lives and economies at catastrophic risk, Hamburg and Poland said. "No one will do this for us; we must do it together, and the roadmap provides the action steps and timelines to get us there."

Knowledge gaps and other challenges
Developing better vaccines first depends on a better understanding of the global distribution of coronaviruses, and the CVR sets out a plan for coordinated and sustained efforts to collect them and to characterize the full range of reservoirs in wild and captive animals. The results will help scientists pick the viruses to include in broadly protective vaccines.

Linfa Wang, PhD, a member of the CVR task force and zoonotic disease scientist at Duke-NUS Medical School in Singapore, said the task is an enormous one that will require long-term commitment and international collaboration. "The coronavirus diversity in bats is so great that we even don't know how much we really know about them."

Another challenge is the rapid evolution of coronaviruses, clearly evident from the variants of concern that result from human infections and a process that also occurs in animals, he said. "It is therefore not enough to do animal surveillance for coronaviruses at one time point; longitudinal surveillance is key."

Little brown bat
University of Illinois, Steve Taylor / Flickr cc
Useful information can only come from active and transparent international collaboration, Wang said. "As the cliché says, viruses recognize no borders, and neither do bats!"

Another tough challenge spelled out in the CVR is the need to better understand the body's immunologic response to both infection and vaccination, especially to identify the factors that promote long duration and broad protection. Teasing out correlates or markers of protection will help speed the development of coronavirus vaccines that use different approaches.

"Improved understanding of the role of immune imprinting from prior infection and vaccination will be critical to advance new vaccine R&D," the group emphasized in the CVR.

Vaccine options, R&D issues
In the in-depth section about vaccines, the group tackled a range of issues, from sketching out ideal profiles of what next-generation vaccines would look like to weighing the extra complexities of developing and making a broadly protective vaccine.

Improved understanding of the role of immune imprinting from prior infection and vaccination will be critical to advance new vaccine R&D.
CVR authors

In the Vaccine summary, the CVR group raises the possibility of making a universal coronavirus that could be stockpiled and used as needed. However, they also described a "tiered approach," starting with a variant-proof SARS-CoV-2 vaccine, then working up to vaccines that protect against broader coronavirus families, starting with sarbecoviruses and working up to betacoronaviruses, then all four genera.

Also, the CVR outlines clinical trial challenges, such as how to compare vaccines with each other and the need to navigate thorny issues preexisting immunity and immunity in participants.

Given that research and development is a main theme, the CVR explores animal models, and even controlled human trials, that could help speed clinical development.

Dan Barouch, MD, PhD, a CVR task force member and professor of medicine at Harvard Medical School, said, "This was a fantastic and open collaborative process among many scientists, physicians, and stakeholders." He also directs the Center for Virology and Vaccine Research at Beth Israel Deaconess Medical Center.

This was a fantastic and open collaborative process among many scientists, physicians, and stakeholders.
Dan Barouch, MD, PhD

He added that the consensus document is a blueprint on the scientific gaps that need addressing to protect against COVID-19 and future pandemics. "The challenge now will be to enact this proposed plan."

Digging into policy and financing
In the section on policy and financing, the group said a big challenge is shrinking support for large-scale vaccine investments, now that the emergency phase of the COVID-19 pandemic has mainly passed. They also identified lack of corporate incentives, uncertainty around public demand for a broadly protective vaccine, and the feasibility of expanding vaccine production capacity as other tough issues to address.

One milestone for addressing financing issues is establishing value assessments or cost-benefit analyses for the next vaccines, starting with variant-proof SARS-CoV-2 vaccines. Another is to convene a stakeholder meeting to look at strategies for building a reliable marketplace and financial model for developing and producing broadly protective coronavirus vaccines.

On April 20, the CVR team will hold a 1-hour scientific webinar that will be open to the public.

In a press release from the University of Minnesota, Gellin, who has led several federal vaccine initiatives and has been a technical advisor for groups including Gavi, the Vaccine Alliance, COVAX, and the World Health Organization, sounded an optimistic note. "Time and time again, we have seen that investment in science brings solutions. The COVID-19 pandemic galvanized the research community and advanced vaccine R&D efficiently and through broad collaborations."


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Potential new treatment for COVID-19 is made from plants
Originally published on MedicalXpress Breaking News-and-Events


Viruses, including SARS-CoV-2, use an extensive arsenal to help them cleverly evade the immune system, proliferate and cause disease. Among their formidable weapons is the ability to ceaselessly mutate, developing new variants that the body's natural or vaccine-induced defenses cannot fight.

In new research, Shawn Chen, a researcher with Arizona State University's Biodesign Center for Immunotherapy, Vaccines and Virotherapy and School of Life Sciences, describes an innovative therapy for COVID-19. The method highlighted in the study uses transient expression in tobacco plants to develop and produce a monoclonal antibody, or mAb.

The crucial advantage of the therapy is that it may protect against COVID-19, even as the virus attempts to evade immune detection through mutation. The novel coronavirus SARS CoV-2 is responsible for the COVID-19 global pandemic. A new form of monoclonal antibody therapeutic to treat the disease is described in a new study, which graces the cover of Plant Biology Journal.

The treatment could be particularly useful for elderly patients and people with compromised immune systems who are highly vulnerable to SARS-CoV-2 and its emergent variants. The new therapy could also be added to existing therapies for COVID-19, significantly enhancing their protection. Further, using plants to produce therapeutics offers several advantages over conventional methods, including reduced cost, safety and speed of development.

High-potency, multipurpose therapy

The first monoclonal antibodies were developed in the 1970s to target cancer. They have since been engineered to combat a wide range of diseases and are a powerful tool in the fight against the novel coronavirus causing COVID-19.

While there are four classes of monoclonal antibodies, nearly all successful mAb therapies for COVID-19 have relied on class 1 or 2. The new therapy, a class 4 mAb, provides some key advantages over existing treatments.

"This monoclonal antibody treatment is mostly mutation resistant, and it neutralizes several variants, including Omicrons. This provides a therapeutic candidate for fighting against new mutations of the COVID-19 virus," Chen says. "The approach provides a universal cocktail partner to boost approved emergency use authorization therapeutics for treating COVID-19, especially current and future variants that are resistant to current monoclonal antibody treatment."

Because the research describes a different monoclonal antibody mechanism of action, it also advances basic knowledge of how mAbs work against SARS-CoV-2 infection.

The new research has been selected for the cover of the current issue of Plant Biotechnology Journal.

Beyond ACE2

During COVID-19 infection, the virus's spike protein fuses with a receptor on the cell's surface, known as ACE2. The binding of the virus to ACE2 is a crucial step in the process of viral entry into host cells, and this interaction is targeted by many antiviral therapies, including most monoclonal antibodies.

The ACE2 binding site is highly conserved among different SARS-CoV-2 variants, although mutations in this region can occur and may affect the virus's ability to enter cells and their success at thwarting vaccines or therapeutics designed to target them.

The ACE2 receptor is expressed in various tissues throughout the body, including the lungs, heart, kidneys and intestines, which may contribute to the diverse symptoms and complications associated with COVID-19.

Monoclonal 2.0

Monoclonal antibodies are laboratory-made molecules that can mimic the immune system's ability to fight off pathogens, including SARS-CoV-2 and other viruses. They are designed to bind specifically to a target protein or antigen, which in the case of SARS-CoV-2, is usually the spike protein's receptor-binding domain on the viral surface.

By blocking the virus's entry into human cells, reducing viral load and triggering the immune system to fight off the infection, monoclonal antibodies can help reduce the severity of COVID-19. The class 1 and 2 mAbs, now commonly used against COVID-19, are highly potent and can neutralize a specific variant of the virus by targeting the receptor-binding domain of the SARS-CoV-2 spike protein. Nevertheless, the virus can sometimes manage to outmaneuver such therapies.

One way SARS-CoV-2 can accomplish this is by modifying the spike protein's ACE2 receptor-binding domain through mutation. The effect of these alterations may be to increase or decrease infectivity. They may also affect the severity of the disease caused by the virus, or the virus's ability to evade the immune system.

This is where the monoclonal antibody described in the new study comes in. Rather than binding with the ACE2 receptor-binding domain, the novel class 4 monoclonal antibodies target a site that is distant from the ACE2 binding domain yet can effectively neutralize multiple variants of concern, including Omicron variants.

This innovation provides an important advantage. Because the binding domain targeted by the new monoclonal antibody treatment is not under strong selective pressure, it is mutation resistant, compared with ACE2, making it much harder for the virus to outwit the therapy.

Power in plants

The study highlights the potential of synergizing antibody cocktails with the addition of monoclonal antibodies that do not directly hinder ACE2 binding to the receptor-binding domain. The study also underscores the potential of plant-based monoclonal antibody expression platforms in therapeutic development against the ever-evolving SARS-CoV-2 pandemic.

Plant-made COVID-19 therapies have several advantages over other production platforms. Plants can produce large quantities of therapeutic proteins in a relatively short amount of time, making them ideal for scaling up production. They are inexpensive to grow and maintain, making them a cost-effective alternative to traditional protein expression systems. Because plants are not natural hosts for human pathogens, their use reduces the risk of contamination with infectious agents.

Finally, plant-based expression systems can be rapidly reprogrammed to produce new therapeutics in response to emerging pathogens such as SARS-CoV-2, making them an attractive option for pandemic response.

This article was originally published on MedicalXpress Breaking News-and-Events.

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The latest​

House Republicans overseeing pandemic probes are expanding their investigation into the origins of covid-19, after the Energy Department concluded with “low confidence” that the virus was most likely spread via an accidental laboratory leak in China, my colleague Dan Diamond reports.​

The House select subcommittee investigating the coronavirus response sent letters Monday to the Energy Department, State Department and FBI, seeking an array of materials and interagency communications on the origins of the pandemic and government-funded research. The subcommittee is scheduled to hold its first hearing on the origins question on Wednesday.

The Energy Department, initially undecided about the virus’s origins, changed its view about the likely cause of the pandemic following a new analysis by experts from the U.S. national laboratory complex — including members of a little-known scientific team known as Z-Division, which specializes in emerging security threats, The Washington Post’s Joby Warrick, Ellen Nakashima and Shane Harris report. But within the administration, federal agencies remain divided over which theories they lean toward, with more favoring the natural transmission hypothesis.

The Washington Post’s Joel Achenbach was out with a deep dive this week into the two main theories about the origins of the pandemic, including what we know and what remains a mystery.​

U.S. officials have disclosed little new or compelling scientific information about the cause of the pandemic, despite the debate that came roaring back to life this week in light of the Energy Department’s updated assessment, Joel notes.

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As it stands, there are two main theories about how the pandemic began. One is natural origin, a hypothesis favored among scientists, because pandemics have historically started with viral spillover. Essentially, this theory posits that the virus was transmitted from an animal to a human, probably at the Huanan Seafood Market in the Chinese city of Wuhan. The other is the “lab leak” theory, which asserts there was a laboratory accident at the nearby Wuhan Institute of Virology, which has done extensive work on coronaviruses.

The origin of covid has become so polarizing that an explanation may never emerge that results in widespread satisfaction, Joel writes. Because the issue is politicized, it is vulnerable to motivated reasoning — interpreting facts to fit a preferred narrative. Read more from Joel’s FAQ here.

Other important news​

President Biden is calling on Congress to approve $1.6 billion to combat a “historic” level of fraud targeting the federal government’s coronavirus aid programs, my colleague Tony Romm reports. The push could face familiar political obstacles on Capitol Hill, where lawmakers from both parties have ignored repeated requests for new money and greater resources to pursue pandemic wrongdoing.


Gov. Gavin Newsom (D) officially ended California’s covid-19 state of emergency this week, declaring that “the conditions of extreme peril to the safety of people and property … no longer exist.” Such declarations continue in just six other states, including Texas and Illinois, according to the National Academy for State Health Policy, with Delaware’s poised to end Friday.

Pfizer and its German partner, BioNTech, are seeking emergency use authorization of their updated omicron-targeting coronavirus vaccine as a booster dose for children 6 months through 4 years of age, the companies announced this week.

Coronavirus vaccine maker Novavax raised doubts about its ability to remain in business this week, citing serious financial challenges stemming from raw material shortages and manufacturing setbacks as it developed its shot during the pandemic, my colleague Christopher Rowland reports.

Your questions, answered​

Neither myself nor anyone in my family, sister, brother or daughter (works in the medical field) have ever gotten covid. My siblings and I are in our 60s. We have all been fully vaccinated and possibly exposed to someone who has been infected, but we have never gotten sick. I know that we are very, very lucky, but I’m thinking it might be something like genetics. No one in my family across the entire country has gotten sick. Is there an ongoing study that I could join to get some insight on this? — Martha, La.

First, congratulations on dodging covid! Researchers are actively studying the genetics of people who have never been infected with the coronavirus, to learn if a rare group of people is truly immune. More information about the study is here, and a screening questionnaire is linked here.

There is a precedent for the idea that a subset of people might simply be immune. People who have a deletion in both copies of a gene called CCR5 are protected against major strains of HIV, because the virus can’t get into their cells.

But there’s also a hitch. It’s hard to find these people. Some people may have had an asymptomatic infection or never tested positive. Others simply may have been lucky — so far.

“In the initial phases, we had been recruiting people who were not infected by the prior virus variant — and then there was omicron,” said András Spaan, a postdoctoral fellow at Rockefeller University working on the study. “A significant part of the people enrolled in the study turned out to be infected by omicron — turned out they were not resistant.”

If some people really are covid-proof, researchers think they may be quite rare. But figuring out the genetic factors that help protect a few people could help scientists find new ways to protect the larger population.

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Is it time for another shot yet?​

Is a sixth Covid vaccine available or will it be? I had all the vaccines available and have so far managed not to get Covid. -Ann It’s been more than six months since the bivalent booster came on the scene, so it’s natural to wonder if it’s again time to roll up our sleeves. In the US, health officials have consistently told us to re-up our Covid shots to keep immunity levels high. “Vaccines continue to be the most important tool in our arsenal to avoid severe illness and death from Covid,” says Katrine Wallace, an epidemiologist at the University of Illinois at Chicago. Fortunately, staying up to date with those shots may get easier. President Joe Biden, along with others, has advocated for a simpler US Covid vaccine strategy centered around a single, annual shot. Advisers to the Centers for Disease Control and Prevention also discussed the proposal at a meeting last month. Wallace says there are pros to the annual approach. “The many booster recommendations over the past couple of years have been confusing to the public and, as a result, every subsequent booster has had a poorer uptake rate,” she says. Only about 16% of eligible Americans have gotten the bivalent booster released in the fall, even though it’s equipped to specifically target the dominant omicron variant. “The annual booster strategy would help simplify messaging,” Wallace says. “People are already in the habit of getting an annual influenza vaccine in the fall, so the Covid booster could be done at the same time.” Most Americans have received at least one Covid shot, giving them at least some immunity, and newer variants tend to cause relatively mild infections, so annual shots may be enough to protect the average person. But high-risk populations may not feel so comfortable only getting jabbed once a year. “While good arguments can be made in support of the annual shot strategy for most Americans, we do not really know whether this will be enough protection for everyone given waning mRNA vaccine effectiveness over time and the unpredictability of viral mutations,” says Wallace. If you are older or suffer from health conditions that make you more vulnerable to the virus, Wallace suggests talking with your health-care provider about possibly getting vaccinated more frequently. — Kristen V. Brown "

 

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Even Mild COVID Is Hard on the Brain​

Megan Brooks
March 06, 2023




Even mild cases of COVID-19 can affect the function and structure of the brain, early research suggests.
"Our results suggest a severe pattern of changes in how the brain communicates as well as its structure, mainly in people with anxiety and depression with long COVID syndrome, which affects so many people," study investigator Clarissa Yasuda, MD, PhD, from University of Campinas, São Paulo, Brazil, said in a news release.

"The magnitude of these changes suggests that they could lead to problems with memory and thinking skills, so we need to be exploring holistic treatments even for people mildly affected by COVID-19," Yasuda added.
The study was released early, ahead of presentation at the upcoming American Academy of Neurology (AAN) 2023 Annual Meeting in April.

Brain Shrinkage​

Some studies have shown a high prevalence of symptoms of anxiety and depression in COVID-19 survivors, but few have investigated the associated cerebral changes, Yasuda told Medscape Medical News.



The study included 254 adults (177 women, 77 men, median age 41 years) who had mild COVID-19 a median of 82 days earlier. A total of 102 had symptoms of both anxiety and depression and 152 had no such symptoms.


On brain imaging, those with COVID-19 and anxiety and depression had atrophy in the limbic area of the brain, which plays a role in memory and emotional processing.

No shrinkage in this area was evident in people who had COVID-19 without anxiety and depression or in a healthy control group of individuals without COVID-19.

The researchers also observed a "severe" pattern of abnormal cerebral functional connectivity in those with COVID-19 and anxiety and depression.


In this functional connectivity analysis, individuals with COVID-19 and anxiety and depression had widespread functional changes in each of the 12 networks assessed, while those with COVID-19 but without symptoms of anxiety and depression showed changes in only 5 networks.

Mechanisms Unclear​

"Unfortunately, the underpinning mechanisms associated with brain changes and neuropsychiatric dysfunction after COVID-19 infection are unclear," Yasuda told Medscape Medical News.


"Some studies have demonstrated an association between symptoms of anxiety and depression with inflammation. However, we hypothesize that these cerebral alterations may result from a more complex interaction of social, psychological, and systemic stressors, including inflammation. It is indeed intriguing that such alterations are present in individuals who presented mild acute infection," Yasuda added.


"Symptoms of anxiety and depression are frequently observed after COVID-19 and are part of long-COVID syndrome for some individuals. These symptoms require adequate treatment to improve the quality of life, cognition, and work capacity," she said.


Treating these symptoms may induce "brain plasticity, which may result in some degree of gray matter increase and eventually prevent further structural and functional damage," Yasuda said.


A limitation of the study was that symptoms of anxiety and depression were self-reported, meaning people may have misjudged or misreported symptoms.


Commenting on the findings for Medscape Medical News, Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, Missouri, said the idea that COVID-19 is bad for the brain isn't new.


As previously reported by Medscape Medical News, early in the pandemic, Raji and colleagues published a paper detailing COVID-19’s effects on the brain and Raji followed it up with a TED talk on the subject. (Raji wasn't involved with Yasuda's team for this current study.)


"Within the growing framework of what we already know about COVID-19 infection and its adverse effects on the brain, this work incrementally adds to this knowledge by identifying functional and structural neuroimaging abnormalities related to anxiety and depression in persons suffering from COVID-19 infection," Raji said.


The study was supported by the São Paulo Research Foundation. The authors have no relevant disclosures. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution LLC.


American Academy of Neurology (AAN) 2023 Annual Meeting: Abstract 1998. To be presented April 24, 2023.


Medscape Neurology news

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A new class of drugs could prevent resistant COVID-19 variants, study finds
Published March 9, 2023 | Originally published on MedicalXpress Breaking News-and-Events

The constant evolution of new COVID-19 variants makes it critical for clinicians to have multiple therapies in their arsenal for treating drug-resistant infections. Researchers have now discovered that a new class of oral drugs that acts directly on human cells can inhibit a diverse range of pathogenic SARS-CoV-2 strains.

In their newly published study, the team found a novel mechanism through which the gene that expresses angiotensin converting enzyme-2 (ACE-2)—the cellular receptor to which SARS-CoV-2 binds so that it can enter and infect the cell—is turned on. They also found that a class of oral drugs currently in human clinical trials can block this pathway and potentially be a therapeutic for all SARS-CoV-2 variants, as well as any newly emerging SARS-like viruses. The team published its findings in Nature Genetics.

"Because of drug-resistant variants, we're down to only one drug, Paxlovid, as far as our oral options," says Craig Wilen, MD, Ph.D., associate professor of laboratory medicine and of immunobiology, and a member of Yale Cancer Center.

"Targeting these master regulatory complexes complements existing approaches and fills a need for a new drug class that can be exploited to help combat drug resistance and infection." Wilen and Cigall Kadoch, Ph.D., of Dana-Farber Cancer Institute, were co-senior authors of the study.

Researchers identify mSWI/SNF complexes and as potential anti-viral targets

In a previous study published in 2021, Wilen's team at Yale performed genetic screening to identify host factors that are essential for SARS-CoV-2 infection. One of the key players was the mammalian switch/sucrose non-fermentable (mSWI/SNF, also called BAF) chromatin remodeling complex, a group of over a dozen very conserved proteins that allow certain genes to turn on.

"At that point, I'd never heard of it in the setting of virus infection, and we couldn't understand why it was important for coronaviruses," says Wilen. Thus, the group teamed up with experts on this complex, the Kadoch Lab at the Dana-Farber Cancer Institute and Harvard Medical School to find out how the protein complex acts to make cells susceptible to infection and if newly emerging drugs against these complexes could stunt viral infection.

At the time they embarked on their collaborative work, the U.S. Food and Drug Administration had authorized six monoclonal antibody treatments for emergency use, yet none of these treatments work against the newest Omicron variants.

This leaves clinicians with remdesivir, which can only be administered through an IV, limiting its use; molnupiravir, an oral drug that works similarly to remdesivir but only has 30 percent efficacy; and Paxlovid, an oral antiviral that works through inhibiting the viral protease. Paxlovid, Wilen says, is the mainstay of current treatment.

"It's a great drug that works well, but there has been some emerging drug resistance to it," he says. "And currently, that is the only drug in our toolbox that we can give as an oral form." The dwindling of effective treatments further highlights the critical need for a new class of drugs to add to the toolbox, and ideally, ones that are less susceptible to quick-acting resistance mechanisms.

Blocking mSWI/SNF protects cells against SARS-CoV-2

First, the team discovered that disrupting mSWI/SNF complexes prevented viral entry into human cells. Because mSWI/SNF is known to regulate genes turning on and off, they then hypothesized that it might also play a role in activating the ACE-2 receptor. Next, they uncovered its mechanism: mSWI/SNF binds to another protein called HNF1A, a transcription factor, which directs it to the gene that encodes ACE-2.

Upon disrupting mSWI/SNF complexes, the cell could no longer make ACE-2 and became resistant to infection by any virus that uses that receptor. This includes many coronaviruses.

Small molecule inhibitors that target mSWI/SNF have already been developed by Kadoch-founded Foghorn Therapeutics and are in phase I clinical trials as a therapeutic for several cancers. Wilen and Kadoch found that this class of drugs was effective against multiple variants of SARS-CoV-2—including a remdesivir-resistant strain isolated from a Yale patient—without any adverse effects on the cell. "This is proof of principle that this can be a really important first- or second-line tool to combat drug resistance," says Wilen.

"Further, this speaks to the wide, multi-disease potential for pharmacologic modulation of chromatin remodeling complexes," says Kadoch. "These molecular machines sit at the top of the pyramid in governing gene expression programs that go awry in many different human diseases—we are just at the tip of the iceberg in identifying and exploring their utility."

Wilen believes the drugs in these clinical trials can potentially be repurposed to inhibit both current and future coronaviruses. Furthermore, Wilen and Kadoch hope the work can provide insight into why certain people and specific cell types may be more susceptible to coronavirus than others. "Future work is needed to look at the underlying biology of why some people are asymptomatic while others experience severe infection and death," Wilen says.

COVID-19 will not be the last severe viral outbreak. Wilen's lab studies coronaviruses circulating in wild bats, which he believes pose the highest risk for infecting humans and causing the next pandemic. Many of these viruses use ACE-2 as a receptor, which means that this new study may hold the key to slowing or stopping the next outbreak.

"We're going to have another pandemic, whether it's in a few years or a decade. And we're underprepared for it," he says. "The best way to prepare is to have as many vaccines and drugs as possible ready to go so that we can combat the outbreak early with maximum effectiveness."

This article was originally published on MedicalXpress Breaking News-and-Events.
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Three years ago tomorrow, the World Health Organization declared the spread of what was then called the novel coronavirus to be a pandemic. Some 4,200 Covid-19 deaths had been confirmed at that point. Almost 7 million would follow, though the true number of lives lost is believed to be much higher. In March of 2020, the pathogen had already spread to more than 100 countries. Horrific waves would sweep across Europe and the US, which for much of the pandemic suffered the worst death toll of all. No part of the planet would be untouched, as India later suffered a crushing surge and, more recently, China after the sudden lifting of precautions. The constant wail of sirens that punctured the night in cities like New York—an initial epicenter of the global disaster—has receded. But with close to 1,000 confirmed Covid-19 deaths every day all over the world, the pandemic isn’t over. —David E. Rovella

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The latest​

U.S. officials relaxed coronavirus testing requirements on travelers from China on Friday, a sign of diminished concern about covid transmission from that country.​

National security and health officials had reached a decision earlier in the week to roll back the testing requirements, which our colleague Dan Diamond first reported in a scoop. Three officials had told Dan the decision was driven by public health, rather than foreign policy, priorities. Other countries, such as Japan, have also eased similar testing rules.

The Centers for Disease Control and Prevention issued a statement offering details of the move, which went into effect at 3 p.m. Friday. “This means that … air passengers will no longer need to get tested and show the negative COVID-19 test result, or show documentation of recovery from COVID-19, prior to boarding a flight to the U.S. from the People’s Republic of China, Hong Kong, and Macau, or through a Designated Airport,” the statement said. The designated airports include Incheon International Airport in Seoul, Toronto Pearson International Airport and Vancouver International Airport.

​

​ ​

​

The testing requirement was put in place two months ago, when the end of China’s zero-covid policies sparked a surge in covid cases and deaths in the country. At the time, U.S. officials were concerned that the wave of cases sweeping China could spark new variants that might threaten other countries. The policy was also intended to put pressure on China to more aggressively monitor and share data amid questions about the country’s implausibly low numbers of covid cases and deaths, Dan writes.

During the last three years, conservative and libertarian forces have stripped public health officials of their powers. In passing laws and winning lawsuits, they’ve had a string of victories in Republican-led states that could have major ramifications for future outbreaks, my colleagues Lauren Weber and Joel Achenbach report.​

Health officials and governors in at least 30 states are now restricted from issuing mask mandates, ordering school closures and imposing other public health measures. To renew emergency orders, they will have to get approval from state legislatures, almost all of which are led by GOP lawmakers, according to a new analysis from Lauren and Joel.

The movement to curtail public health powers was driven by widespread frustration among the public over the government’s inconsistent and contradictory guidance during the pandemic. Among the mistakes: a reversal on whether people should wear masks, confusing messages on when to stop isolating after an infection and the duration of school closures.

As the nation enters its fourth year with covid, what emerges is a portrait of a public health system that has been largely defanged, Lauren and Joel write. The result, public health experts warn, is a battered patchwork system that makes it harder for leaders to protect the country from infectious diseases that cross red and blue state borders.

Other important news​ California Gov. Gavin Newsom (D) has tested positive for covid for the second time in less than a year after exhibiting mild symptoms, his office announced Wednesday. He will work remotely and self-isolate for at least five days, Laurel Rosenhall reports for the Los Angeles Times. New York Mayor Eric Adams (D) is calling on shop owners to require customers to briefly remove their face masks when entering stores to help law enforcement crack down on retail crime, according to Liam Stack at the New York Times. The House select subcommittee on the coronavirus pandemic kicked off its investigation into the origin of the virus this week with a hearing that produced no new evidence but offered plenty of political theater. During the hearing, House Republicans aggressively pushed the theory that the virus leaked from a laboratory in Wuhan, China, while acknowledging there is still no definitive evidence to support how the pandemic began, Shannon Pettypiece reports for NBC News.​ ​ ​ ​ ​ Your questions, answered​ What is the risk of getting covid from giving someone a brief hug while being outside? I am a 65-year-old female with no health conditions and up to date on all coronavirus vaccinations and boosters. I think the risk is negligible, and my friend disagrees and thinks I am breathing their cloud of exhaled air. I will continue to wear a mask indoors, but not to give a friend a hug while outside seems unreasonable — Judy, Calif. Good news: Infectious-disease experts take your side. “You can never say never about transmission,” but the risk of infection in the situation you describe is negligible, said Jeanne Marrazzo, director of the division of infectious diseases at the University of Alabama at Birmingham. Transmission of the virus depends on proximity to individuals who are infected, how forcefully they are expelling their breath and the duration of your exposure, she said. In other words, the risk of a brief hug outdoors is minimal. “Plus,” she added, “you have to balance any tiny risk against the benefits of a hug. We didn’t get enough hugs during the pandemic.” Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine, agreed, saying that while “the risk of transmission is never zero,” the risk is very low — “especially if you are not kissing the person.” Hotez added that you could be extra careful by turning your head to the side during the hug. And you could always wear a mask, but he didn't believe that was practical or necessary.​

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'COVID rebound' is common, even in untreated patients, reports study
Published March 6, 2023 | Originally published on MedicalXpress Breaking News-and-Events

"COVID rebound," in which evidence of the illness disappears and then returns days or weeks later, is surprisingly common—whether or not patients are given the antiviral Paxlovid.

The results, reported on February 22 in Clinical Infectious Diseases by scientists at Scripps Research and the digital health company eMed, are a preliminary readout from an ongoing observational study of people who order SARS-CoV-2 antigen test kits online.

The researchers found that in an initial group of 170 eMed Test-to-Treat kit users, the disappearance and then return of evidence of the virus on antigen tests and in self-reported COVID-19 symptoms occurred in 9.3% and 7.0% of patients who opted not to take antiviral treatment, and in 14.2% and 18.9% of those who opted for Paxlovid.

Although a higher proportion of the Paxlovid-treated group reported COVID-19 rebound, the difference was not statistically significant in this early snapshot of the ongoing study, which is designed ultimately to enroll a total of 800 patients.

"These preliminary results suggest that rebound after clearance of SARS-CoV-2 test positivity or COVID-19 symptom resolution is more common than previously reported in both treated and untreated patients," says study lead author Jay Pandit, MD, an assistant professor and director of Digital Medicine at the Scripps Research Translational Institute. "We're going to need a larger set of participants and more extended follow-up to better understand this rebound phenomenon."

The study, conducted from August to November of last year, was a collaboration with eMed, including epidemiologist and Chief Science Officer Michael Mina, MD, Ph.D., previously professor at Harvard T.H. Chan School of Public Health, and others at the Test-to-Treat company, which is also implementing the NIH Home Test to Treat COVID-19 program.

Reports of COVID-19 rebound started appearing in the medical literature in 2022. The cause of rebound has been unclear, although the suggestion in most of these reports has been that rebound occurs more often in patients treated with Paxlovid. The latter, a mix of two antiviral compounds (nirmatrelvir and ritonavir), received emergency use approval in late 2021 from the U.S. Food and Drug Administration (FDA) for treating patients who have mild-to-moderate COVID-19 and are at high risk of developing severe COVID-19.

To help illuminate the rebound phenomenon and any connection to Paxlovid, Pandit and his colleagues teamed up with eMed to drive a "real-world" study of outcomes among people using the company's COVID-19 Test-to-Treat antigen test kits with telehealth proctoring and telemedicine.

"As the COVID-19 landscape continues to evolve, the importance of making timely and effective treatments accessible and thereby helping reduce severe disease outcomes cannot be overstated," Mina says.

"Collaborations such as this with the Scripps Research Translation Institute are a key part of efforts to gather evidence-based data and answer critical questions associated with treatment outcomes. We are also proud that this study not only offers new data surrounding COVID-19 recovery and treatment outcomes, but also highlights the benefits of industry and academic partnerships to accelerate high-quality public health and translational research."

The researchers offered Test-to-Treat telehealth kit users participation in the study if they had a verified positive test. If users consented to participate, the researchers sent them more test kits, and asked each participant to take a test and fill out a symptom questionnaire every other day for 16 days. The team then compared the rates of rebound for those who did and didn't opt to take Paxlovid.

Rebound was measured in two ways: a positive test result after a negative test, or a reported recurrence of symptoms after symptom resolution. For this preliminary analysis, there were 127 people in the Paxlovid-treated group, and 43 in the non-Paxlovid group.

Either way rebounds were measured, the Paxlovid group experienced them at a higher rate: 14.2% vs. 9.3% for antigen test rebounds, and 18.9% vs. 7.0% for symptom rebounds. With the small participant numbers included in this preliminary analysis, these differences were not statistically significant.

Moreover, on other measures (such as the time from first positive antigen test to first negative antigen test, and time from symptom onset to first symptom resolution), the two groups had essentially identical outcomes. Age, gender and pre-existing conditions also did not appear to influence rebound.

Pandit emphasizes that the study is not currently powered to detect statistically significant results, and a final analysis should include up to 800 participants and thus should have much more power to generate conclusive findings. However, he adds, the preliminary findings already make clear that the rebound rates for both treated and untreated groups are higher than the rates reported in prior studies.

For example, an analysis of their clinical trial results by Pfizer, the maker of Paxlovid, found rebound rates of only about 2% in both Paxlovid and placebo groups over a two-week period.

In addition to increasing the number of participants in their ongoing study, Pandit and colleagues plan to start sequencing the virus found in participants and testing participants' blood samples for antibody levels and other immune markers.

"We're hoping to answer key questions about the rebound phenomenon, such as whether it's enhanced by Paxlovid, how much it depends on the viral variant and what is the role of the patient's immune system," Pandit says.

He and his team also plan to improve the balance of ethnic and racial representation between the treatment and control groups: In the initial group of 170, Whites were much more likely than Blacks and Latinos to opt for Paxlovid treatment.
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I need some Covid safety tips for the gym​

I am thinking of going back to the gym and wondering if public health folks have any advice for making it less risky? Emma, Brooklyn, NY Well, dear reader, you’re a better woman than I. For me, the pandemic was an excuse to quit the gym permanently and replace my membership with a Peloton. I often admire my bike from a distance while sometimes even wearing workout clothes. Gyms can be especially risky spaces during a pandemic because people breathe more heavily when they’re exerting themselves, expelling respiratory particles at a greater range. Additionally, in the gym, you’re often near others and touching the same surfaces. A few things can make the experience safer. “First, make sure you are up to date with your vaccines. If you never got around to getting the bivalent Covid vaccine, this is the time,” says Jessica Justman, an infectious disease specialist and epidemiologist at Columbia University Irving Medical Center. A mere 16% of eligible Americans have gotten this shot, so seriously, check if you have. It will help minimize your risk of severe illness if you catch Covid while getting swole — or any other time. “Then adjust your timing so that you go to the gym at off-peak hours,” Justman says. Keeping your distance from others or exercising outside can help, too. Justman recommends wearing a mask at the gym, if you can tolerate it, and checking on the facility’s Covid policies. “Wiping down mats and equipment is a plus but in my view is not enough on its own,” Justman says. “Did the gym upgrade its ventilation in response to the pandemic? Detailed guidance on ventilation and Covid on the CDC website is helpful for gym owners.” One gym made headlines in 2020 after one of its members helped it avoid a major viral outbreak this way. Linsey Marr, an expert on airborne disease transmission, advised it on upgrading its ventilation system. Later a coach there got Covid but none of the 50 athletes he’d trained were infected. — Kristen V. Brown

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More Young Kids Can Get Bivalent COVID Booster​

— Pfizer's booster authorized in children under 5 who received three doses of monovalent vaccine​

by Kristina Fiore, Director of Enterprise & Investigative Reporting, MedPage Today March 14, 2023


More children under age 5 are now eligible for a COVID-19 booster, the FDA announcedopens in a new tab or window on Tuesday.

Kids ages 6 months to 4 years who completed their primary vaccination with three doses of the monovalent Pfizer-BioNTech shot can now get a booster with the companies' bivalent COVID vaccine -- which targets the Omicron BA.4/5 subvariants -- as long as 2 months have passed, the agency said.

"Today's authorization provides parents and caregivers of children 6 months through 4 years of age who received the three-dose primary series with the monovalent [Pfizer shot] an opportunity to update their children's protection by receiving a booster dose with the [bivalent vaccine]," Peter Marks, MD, PhD, director of the FDA's Center for Biologics Evaluation and Research (CDER), said in a statement.



Since December 2022opens in a new tab or window, children in this age group who got their first two doses with the companies' monovalent shot could complete their three-dose primary series with the bivalent vaccine. (At the time, Moderna's bivalent vaccine was authorized as a booster dose as well, for kids ages 6 months to 5 years following a two-dose primary series.)

Children who have received Pfizer's bivalent vaccine as their third dose will not be eligible for a booster dose of a bivalent vaccine at this time "and are expected to have protection against the most serious COVID-19 outcomes," according to an agency press release.

The updated emergency use authorizationopens in a new tab or window to allow for the fourth dose comes after reviewing immune response data from 60 children in this age group who had three doses of the monovalent vaccine and a bivalent booster, FDA said.

One month after the bivalent booster, these kids "demonstrated an immune response to both the original SARS-CoV-2 virus strain and to Omicron BA.4/BA.5," the agency said in its release.



Evidence of safety of a bivalent booster dose in this age group comes from previous data, FDA said, including studies evaluating the safety of an original strain/BA.1 booster in adults age 55 and up; the monovalent primary series in kids 6 months and older; monovalent boosters in those age 5 and up; and postmarketing safety data with the monovalent and bivalent shots.

Additional safety data come from two clinical studies involving pediatric patients that showed no new safety concerns and no previously unrecognized side effects with a bivalent booster, the FDA said.

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Catch up quick: Long COVID​

KATELYN JETELINA MAR 14

COVID-19 is not the common cold. Here’s an effort to keep you up-to-date on long COVID developments.

Not “in the clear” after first infection​

• What we knew: Long COVID after first infection was clearly a risk. The risk of long COVID-19 after re-infection was not known.
• New info: In the U.K., risk of long COVID dropped after second infections compared to first infection (4% → 2.4%). This is good and bad news: Risk drops, but risk is clearly not zero.
• Why it matters: There is still reason to avoid COVID-19, even if you’ve had it already.

​

Metformin may work​

• What we knew: ~300 clinical trials are testing treatments for long COVID-19, including Metformin. Results are trickling in.
• New info: Metformin reduced long COVID in a large randomized control trial.
  • Metformin had a 42% reduced risk in long COVID cases compared to the placebo; 63% reduced risk if taken within 4 days of symptoms.
  • For every 100 people who took the drug, 4 fewer cases of long COVID 9-months after infection occurred.
  • Ivermectin and fluvoxamine had no impact.
• Why it matters: People should consider Metformin, especially women who are at higher risk for long COVID. It’s best taken within 4 days of infection. This is a challenging timeframe in the U.S. medical care system, though.

​

Cumulative incidence curve of long COVID diagnoses over 10 months after randomization. Source: Lancet preprint.

Paxlovid may help… a little?​

• What we knew: Paxlovid helps reduce severe disease by 50-90%. We didn’t know if it helped with long COVID, though.
• New info: Paxlovid reduced risk of long COVID by 26%, regardless of vaccination status and history of prior infection. We need more studies, particularly among young people, as Paxlovid’s effect will likely increase among younger people.
• Why it matters: There may be small, proxy benefits from taking Paxlovid, including among younger populations that aren’t “eligible.”

Long COVID is annoyingly stubborn​

What we didn’t know: We didn’t know the longevity of severe symptoms.

New info: Among those with long COVID, the rate in which symptoms affected daily life decreased from 45% → 25% over 7 months.

Why it matters: If you get severe long COVID, there is a chance that symptoms will get better after 7 months. Then again, there’s a chance that they won’t.

Still not convinced?​

What we know: People living with long COVID report profound stigmatization because people disbelieve that long COVID is a “thing.”

New info: A YLE community member, Dianna Cowarn (also known as Physics Babe on YouTube), was diagnosed with long COVID last summer. Her crew made a 4-min video. Check it out here if you’re still not convinced. It’s painstaking.

Bottom line​

COVID-19 infection is not the common cold for some. Our knowledge is inching closer to treatments. But with so much unknown, we still need to emphasize prevention—keeping COVID-19 cases low and ensuring vaccination.



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The rate of Americans dying while giving birth — or in the weeks after — increased by more than one-third in 2021 compared with a year earlier, our colleague Akilah Johnson reports, citing a federal study released by the National Center for Health Statistics.​

While the new report does not mention the pandemic, maternal health experts said it was natural to assume the coronavirus fueled the rise in maternal deaths. Research has shown that pregnant people infected with the coronavirus have a seven times higher risk of dying compared with pregnant individuals who are not infected, Akilah writes.

Researchers found that the number of deaths jumped to 1,205 in 2021, up from 861 the previous year. The burden of maternal death during the pandemic’s second year disproportionately affected communities of color, though the report said the jump was “significant” for all racial and ethnic groups.

The pandemic turbocharged the push to make America’s streets more pedestrian friendly. As the covid-19 emergency ends, many cities are fighting to make those changes permanent — but not everyone is happy about it, The Washington Post’s Reis Thebault reports.​

Stay-at-home orders and the remote work boom changed the country’s streets suddenly and profoundly in 2020, emptying them of cars as traffic plummeted to unprecedented levels. Local leaders enacted a flurry of changes, liming traffic on roadways and swapping parking spots for outdoor dining tables. Now, three years later, major U.S. cities have doubled down on plans to restrict driving on main streets, investing in public transit projects and hundreds of miles of new bike lanes.

But a reliance on cars for work and life is ingrained in the DNA of most Americans, and there has been vigorous pushback. “Newly proposed bike lanes have become politically explosive and cities have struggled to formalize once-popular streeteries. Business owners worry that fewer parking spaces means fewer customers. Some warn of gentrification, others of gridlock. With traffic returning to pre-virus levels — and bringing with it an alarming rise in pedestrian deaths — the future of America’s streets still hangs in the balance,” Reis writes.

Other important news​

Pfizer’s antiviral Paxlovid should be approved for the treatment of mild-to-moderate covid in high-risk patients, independent advisers to the Food and Drug Administration recommended Thursday, according to Reuters. Ahead of the meeting, the agency released briefing documents saying the drug is safe, effective and doesn’t cause patients to “rebound” after taking it. The drug has been available under an emergency use authorization issued in December 2021.


The FDA authorized the omicron-targeting coronavirus booster from Pfizer and its German partner, BioNTech, for children who are 6 months to 4 years old. Children in the age group must wait at least two months after completing the three-dose primary series of the company's original vaccine before receiving the updated shot.

Three years into the pandemic, a U.N.-backed program to make mRNA vaccines in developing countries is struggling, my colleague Adam Taylor reports. Its backers are seeking a large increase in funds to ensure long-term sustainability. So far, the United States has offered no money to the program and has yet to respond to a request for $100 million sent late last year.

Your questions, answered​

I can’t take Paxlovid because I have dysphagia. I can’t swallow pills. I’ve read that you can’t chew or dissolve Paxlovid. I’m in my late 70s, vaccinated and boosted, and wear masks inside public places. But this inability to take Paxlovid, should I somehow contract covid, is really concerning! What good alternatives are there for older folks like me, who have trouble swallowing? — Lynn, Ore.

Paxlovid is a widely used antiviral medication that was the first to get Food and Drug Administration emergency authorization to treat covid-19. Yes, it’s only available in pill form — but don’t despair.

While there is currently no approved liquid medication, medical experts say your best bet is remdesivir, which was the first covid-19 treatment to get full FDA approval and is administered by IV infusion. During the early stages of the pandemic, remdesivir was used primarily for hospitalized patients. Research has now shownit’s highly effective at keeping patients out of the hospital if they receive the treatment early.

But it’s not always easy to get treatment. Generally, nurses or doctors will give the IV infusion at a hospital or a specialized clinic. The FDA approved it for outpatient use in early 2022. Tufts Medicine health system in Boston, for example, can arrange for a nurse to visit your home three days in a row to administer the infusion.

“You best bet is to go to your state health department website and find the [covid] treatment page and see what resources the state offers,” said Shira Doron, Tufts’ chief infection control officer, who stressed it’s best to arrange treatment as early as possible after you’ve been diagnosed.

But for people such as the reader, who have taken substantial precautions, there’s a good chance of avoiding becoming infected.

“Vaccinations and boosters reduce the chances of a person ending up in the hospital,” said Dushyantha Jayaweera, a professor of medicine at the University of Miami’s Miller School of Medicine. “It sounds like the [the reader] is doing everything right.”

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The Checkup With Dr. Wen: Three questions that remain after three years of covid

By Leana S. Wen

On March 11, 2020, the World Health Organization officially designated the novel coronavirus as a pandemic. Two days later, then-President Donald Trump declared a national emergency.
The third anniversary of those moments passed by over the past week without much fanfare. President Biden has already said the national emergency for covid-19 will end this May, and most Americans have returned to their pre-pandemic lives.
In this week’s newsletter, I reflect on three remaining questions that scientists and policymakers must continue to address.
How can we protect the most vulnerable?
With covid becoming endemic and no longer a daily consideration for most people, the question of how to safeguard those still at high risk should be the top priority for health officials. This is in line with how we address virtually all other diseases such as HIV and cancer. The priority should be the elderly, the immunocompromised and others who are not able to utilize existing treatments.

Globally, more than 80 percent of covid deaths in 2020 and 2021 occurred among individuals 60 and above. In the United States last year, nearly 90 percent of covid deaths were among people 65 and older. The antiviral Paxlovid is effective in reducing hospitalizations and deaths in this age group, but many cannot take it due to certain medical conditions or because other medications they are taking interact poorly with the drug. And now that the Food and Drug Administration has withdrawn its authorization of the preventive antibody Evusheld, the immunocompromised are left with fewer options.
Over the past three years, we have seen science and public health deliver remarkable successes with a record-setting vaccination campaign. We should marshal this same energy toward developing improved treatments and ensuring that these therapies reach people most at risk.
In the meantime, federal health agencies should allow second bivalent boosters for those who want them. And entities frequented by vulnerable people, such as hospitals and senior centers, should keep in place their mask requirements.
How should we think about long covid?
There is no question that long covid is a serious and often life-changing ailment that affects many Americans. Yet it remains ill-defined and poorly understood.

Research, including a recent Nature paper, increasingly indicates that vaccination can reduce the incidence of long-haul symptoms. Another study, which is online but not yet peer-reviewed, suggests that taking Paxlovid can decrease the likelihood of developing long-term symptoms.
We need far more studies like these. One crucial area of inquiry is what happens with repeat infections, which will almost certainly become more common with covid exposure going forward. We might come to expect some frequency of post-covid symptoms, and the resulting disability, as a “new normal.” In that case, health resources must shift from avoiding the coronavirus to reducing and treating its worst consequences — including long covid.
How do we prepare for the twists and turns ahead?
Covid has not settled into a predictable seasonal pattern. Variants that are currently circulating are all offshoots of the milder and extremely transmissible omicron strain, but it’s entirely possible that a more dangerous strain that can evade the protection of existing vaccines might emerge.

One silver lining from the past three years is the increased attention to disease surveillance. Wastewater testing has proved successful at detecting covid outbreaks early. These efforts should continue so that troublesome variants can be flagged. We also need to renew the urgency to develop vaccines that can cover a broader range of variants.
Then there’s the turmoil from the investigations into covid’s origins. As I’ve argued previously, such inquiries should not delay necessary progress both to improve laboratory safety and to reduce zoonotic transmission. I hope political leaders approach these goals with scientific rigor rather than cherry-picked data points to fit predetermined theories.
For more than three years, covid has been inserted into the partisan culture wars, hindering our response and eroding trust in public health. Covid may no longer be a pandemic, but the impact of the virus itself is far from over. There is much work to be done to protect those still at risk and prepare the United States for future infectious diseases.
Ask Dr. Wen
Newsletter subscribers are invited to submit questions to Dr. Wen. Not a subscriber yet? Click here to sign up.

“I’m 73, immunocompromised and have had all available covid vaccines and boosters. I live alone with no support system and mostly stay in the house, though I do shop for food and run other errands. I always wear a KN94 mask. But I suffer from rhinorrhea, and my nose starts dripping as soon as I put the mask on. What good is it to be in, say, a supermarket, touching all the items, breathing the same air as the largely unmasked other shoppers, if I have to pull off the mask to blow my nose every other minute, with hands that are likely contaminated?” — Sheila from Nevada
A well-fitting, high-quality (N95, KN95 or KN94) mask, when worn properly and consistently, protects against covid and other respiratory diseases. It sounds as if your concern is that you constantly have to take off your mask to wipe your nose. I think the mask can still be protective if you take some additional precautions.
For instance, you should bring hand sanitizer with you and use it before wiping your nose or otherwise touching your nose, mouth or eyes. Bring your own tissues and throw them away after each use, then sanitize again before touching shared public items. You might need to repeat this process multiple times during the shopping trip.

Also, try to be in a part of the store that doesn’t have shoppers around you when you lower your mask. It also helps to go shopping during a time of day that is less busy.
Finally, you might consider discussing your rhinorrhea with your physician. Depending on the cause, there might be medicines you could take that could decrease the discomfort — and anxiety — from the runny nose.
“Are we still in a pandemic? Is it still recommended to test before gatherings?” — Susan from California
These are separate questions. I think there is a case to be made that we are no longer in the pandemic stage of covid-19, but that doesn’t mean we should forego precautions.
If you are vulnerable to severe outcomes from covid, you should consider asking others to test just before seeing you. Taking a rapid, at-home antigen test can catch asymptomatic covid. It won’t catch every case, but every precaution — including home testing and improving ventilation — can reduce the risk of contracting the coronavirus.

“Does covid-19 pose a greater risk to people diagnosed with atrial fibrillation?” — Jane from Connecticut
There are some studies that suggest patients with atrial fibrillation are at greater risk from covid-19. Researchers from Intermountain Healthcare in Salt Lake City found that people with this irregular heart rhythm were more likely to require hospitalization and intensive care. They are also more likely to suffer a major cardiovascular event compared with those who do not have atrial fibrillation. Another study, published in the European Heart Journal, found a similar association.
The more risk factors a person has, the higher their likelihood of severe disease from the coronavirus. If, for example, the heart rhythm abnormality were due to congestive heart failure, the risk would be higher than isolated atrial fibrillation. Those who have diabetes and cancer would also have higher risks.

The Post has also compiled Q&As from my previous newsletters. You can read them here.
What I’m reading
A new study in the Journal of Clinical Oncology found that cancer screening rates are still below where they were pre-covid. Compared with 2019, screening rates for breast cancer in 2021 declined from nearly 60 percent to 57 percent. For cervical cancer, it fell from 45 percent to 39 percent, and for prostate cancer it fell from nearly 40 percent to 36 percent. These decreases were most significant among Asian patients, who saw breast cancer screenings fall 25 percent and prostate cancer testing drop in half. These alarming findings could translate to millions of people at increased risk of missed cancer diagnoses and potentially more advanced cancers.
There is more evidence that natural immunity affords protection from covid. A Lancet meta-analysis of 65 studies from 19 countries found that for at least 40 weeks, the risk of severe covid is about 90 percent lower among previously infected adults compared with their never-infected peers. “Although protection from reinfection from all variants wanes over time, our analysis of the available data suggests that the level of protection afforded by previous infection is at least as high, if not higher than that provided by two-dose vaccination using high-quality mRNA vaccines (Moderna and Pfizer/BioNTech),” the authors wrote.

A randomized controlled trial from Australia published in JAMA Pediatrics found that text message reminders to parents can increase influenza vaccine uptake. About 600 participants, all children with special-risk medical conditions, took part in the study. Nearly 39 percent of parents in the group who received text messages and had clinician reminders vaccinated their children; 26 percent in the group that was reminded by clinicians only did the same. A greater proportion of the group that received text messages also received the vaccine on time, during the optimal seasonable influenza period. “This is an important finding, given the critical importance of timely influenza vaccination for this group,” the authors wrote.

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What’s the deal with natural immunity?​

A new study found previous infections prevent severe Covid infection. How should this impact vaccine policy moving forward? Jason, Chicago When you get a Covid infection it functions a little in the same way a vaccine does. It revs up your immune system to protect you from the virus. The defenses it develops linger in your body. If you encounter Covid again that so-called natural immunity can lower your risk of severe disease, a February meta-study in the Lancet showed. ‘The immunity conferred by past infection should be weighed alongside protection from vaccination when assessing future disease burden from Covid-19, providing guidance on when individuals should be vaccinated,” the authors wrote. That shouldn’t be interpreted as an endorsement for developing immunity to Covid through infection, rather than vaccination, according to Katrine Wallace, an epidemiologist at the University of Illinois at Chicago. “Covid can cause chronic health problems,” she says. “So no one should misunderstand this study to think vaccination in the first place is not important.” She also points out that the study looks at the outcomes of reinfection. That means people who died of Covid aren’t represented in the data, something epidemiologists refer to as “survivorship bias.” The best way to avoid severe infection or chronic infection from Covid is to not get Covid. And the best way to do that is to get vaccinated. New CDC data show the bivalent booster that came out last fall — which only 16% of eligible Americans got — makes a huge difference when it comes to avoiding Covid, according to Wallace. If it’s too late for you to avoid the virus, you should still stay up to date on your shots. Both natural immunity and vaccine immunity wane over time. “Real-world vaccine effectiveness data shows that adults who are vaccinated and receive a bivalent booster are three times less likely to get infected than someone who is unvaccinated, and almost 10 times less likely to die,” Wallace says. — Kristen V. Brown "

 

[missy]

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The latest​

Americans infected with the omicron variant of the coronavirus are less likely to report long-covid symptoms than those who had covid-19 earlier in the pandemic, report my colleagues Amy Goldstein and Dan Keating, citing the largest-ever study of people suffering from lingering effects from the virus.​

One in 12 patients infected with covid-19 during the first wave of the pandemic — from early 2020 to late spring 2021 — suffered persistent symptoms, according to the analysis of nearly 5 million U.S. covid patients conducted by The Washington Post and research partners. By comparison, one in 16 people with omicron received medical care for symptoms associated with long covid within several months of being infected.

The findings also show that patients with certain underlying medical conditions are twice as likely as previously healthy people to seek care for long covid symptoms. Women and older adults are also more prone to report continuing issues. Overall, about 14 million U.S. residents who survived covid-19 continue to struggle with long-lasting effects that often alter their lives, the cause of which remains unknown, The Post’s analysis found.

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Scientists have uncovered new data that may link covid’s origins to raccoon dogs that were illegally traded at a market in Wuhan, China, adding a small but potentially significant data point favoring the notion the pandemic started though a natural spillover from animals to humans, rather than from a laboratory leak, The Washington Post’s Joel Achenbach and Mark Johnson report.​

The new evidence, first reported by The Atlantic, comes from swabs taken from in and around the Huanan Seafood Market in early 2020, shortly after the market had been closed and animals removed. One swab contained a mixture of genetic material from both the coronavirus and a raccoon dog, suggesting the animal may have been an initial host.

Amid a heavily politicized debate about the virus’s origins, this discovery is unlikely to shift the views of those who favor the lab leak theory. The information comes from Chinese scientists who have submitted a paper to a scientific journal that has not yet been published. On Friday, Tedros Adhanom Ghebreyesus, director general of the World Health Organization, renewed his call for China to share its data about the start of the pandemic.
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​ Other important news​ School closures during the pandemic, followed by disputes over masking and other precautions, sharpened existing political and societal divides among parents and school boards, fueling hostility and a new wave of laws across the country restricting what children can learn and do at school, my colleague Hannah Natanson reports.​ Tennis star Novak Djokovic will miss the Miami Open this week after being denied an exemption that would have allowed him to enter the United States despite not being vaccinated against the coronavirus, Ellen Francis reports for The Washington Post. The Transportation Security Administration requires proof of vaccination from international air travelers under a rule in place through at least April 10. Sen. Richard J. Durbin (Ill.), the chamber’s No. 2 Democrat, has tested positive for covid for the second time in the past year. “Thankfully, I am fully vaccinated and boosted and only experiencing minor symptoms,” Durbin said in a tweet.

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[missy]

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Do we need a spring COVID-19 booster? ​

KATELYN JETELINA AND JEREMY FAUST, MD MAR 23

It’s been close to 6 months since the initial rollout of the fall (bivalent) booster. A lot of people are wondering: Do I need a spring booster?

The answer hinges on more questions: What is the purpose of vaccines? Does that purpose change depending on age or health status?

The purpose of the vaccines​

Last month, the FDA and CDC made it clear that the primary purpose of vaccines is to prevent severe disease and death. Decreases in infection and transmission are a bonus at this point, and unfortunately, protection against infection is only temporary.

This makes sense for younger and healthier people. They are staying out of the hospital from COVID-19 for three main reasons:

1. Hybrid immunity. Younger people are more likely to have been infected. People with both vaccination and infection history have protection that lasts longer.
2. Less likely to have comorbidities. Their immune systems are less taxed.
3. Robust immune memories, particularly T-cells. Their thymuses (the organs that give rise to T cells) haven’t gradually degraded into useless blobs of fat, yet.

This means that even if antibodies are waning after 5-6 months, this is okay because protection against severe disease isn’t waning yet.

The story is different for immunocompromised and other very high-risk groups, like older Americans with comorbidities. The purpose of the vaccines for this group should also be to prevent severe disease and death. However, one could argue that in order to do that, we also need to prevent illness.

There’s one big reason for this: SARS-CoV-2 infection can exacerbate potentially fatal underlying illnesses, like heart failure or diabetes. Protection against viruses and underlying illnesses relies on antibodies to act quickly before the immune system is pulled in multiple directions. If it is pulled in multiple directions, it can lead to hospitalization and death.

Immunocompromised​

Of the COVID-19 hospitalizations today, 25% are among the immune-compromised. (Immune-compromised make up 3% of the general population). There are really two subgroups to think about:

1. Non-responders to vaccines. At this point, this is a very small group of people, like organ transplant patients. Some people who did not respond to 2 or 3 doses eventually did respond to 4 or 5 doses. For the remaining non-responders, one could argue that there’s no point in boosting them, but the downsides of trying seem low.
2. Protection wanes quickly. The majority of immunocompromised people belong in this second group. The vaccine works, but just not as well and not as long. For them, vaccine effectiveness against hospitalization with the fourth dose peaks at 51% at 0-2 months, then drops to 28% by 2-4 months. (The bivalent booster may increase protection and duration, but we don’t know yet.)

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Figure from Chemaitelly et al., Long-term COVID-19 booster effectiveness by infection history and clinical vulnerability and immune imprinting. The Lancet Infectious Diseases. Source link here.
There are few downsides to boosting this group every 6 months. It’s actually possible that the immune-compromised are somewhat protected against imprinting by virtue of their sluggish immune systems.

Older Americans with comorbidities​

Those 65 years and older are contributing more and more to the proportion of deaths over time. Among adults hospitalized for COVID-19, 96% had at least one underlying condition.

This is because 2 of the 3 defense walls have more holes than those of younger people. Comorbidities also increase with age, which means the immune response in general is a lot more taxed.

So this is another group in whom we want to prevent infection in order to prevent severe disease.

The latest data from the last ACIP meeting shows waning protection against infection among this group after 4-5 months.

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(ACIP slide)
The good news is that we clearly see that the risk of severe disease even in the very elderly dramatically declines with vaccination. In fact, very few people are in the hospital today who are up-to-date on vaccines. However, will this change with time? How much each booster helps (or does not help) incrementally is something that we really don’t have a good grip on prospectively.

What are other countries doing?​

Canada and the U.K. have offered the bivalent vaccine to the following groups this spring. To our knowledge, this wasn’t based on any new data but rather a similar thought process as above.

Both countries used loose language: people “can” as opposed to “should” get a booster 6 months after the last dose:

U.K.:

• People aged 75 years and older
• Residents of care homes and other living settings for seniors
• Those aged 5 years and older with a weakened immune system

Canada:

• People aged 80 years and older
• Residents of care homes and other living settings for seniors or those with complex medical care needs
• People aged 18 years and older who are moderately to severely immunocompromised
• People aged 65 to 79 years, particularly those with no history of SARS-CoV-2 infection

Will this be needed every 6 months until we start seeing predictable COVID-19 patterns? We don’t know. The WHO is meeting in Geneva this week to discuss global COVID vaccine recommendations going forward.

Bottom line​

If you’re immunocompromised and/or an older adult with a comorbidity (and it’s been 6 months since an infection or last booster), a spring booster may be a good idea to stay ahead of the virus. Will it be official U.S. policy? We don’t know. There are rumors of FDA conversations happening behind closed doors. Hopefully, we will have an answer soon. But, as you can tell, it’s not a straightforward call.

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[missy]

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The latest​ The White House will disband its covid response team after the public health emergency ends in May, my colleagues Dan Diamond and Tyler Pager report.​ “The move to disband the White House covid team, created in February 2020 and expanded to about three dozen staffers under President Biden, comes as the pandemic has receded from U.S. hospitals and in voters’ minds,” Dan and Tyler write. “The nation avoided a feared winter surge of virus deaths earlier this year, and while the Centers for Disease Control and Prevention still links about 2,000 deaths per week to covid, that represents the lowest death toll since the earliest days of the pandemic.” ​ ​ ​ ​ In a statement, a senior administration official said moving out of the emergency phase “is the natural evolution of the covid response.” Ashish Jha, who has served as Biden’s covid coordinator since last spring, is likely to leave the administration once the team shuts down, according to multiple officials familiar with the matter. Some members of the covid response team are expected to join a new White House pandemic response office, which is set to open this year. President Biden signed a bill this week ordering the federal government to declassify some information about the origin of the coronavirus, The Washington Post’s Amy B Wang and Mark Johnson report.​ The Republican-sponsored bill, which received unanimous support in Congress this month, requires the Office of the Director of National Intelligence to declassify all information relating to potential links between China’s Wuhan Institute of Virology and the origin of covid-19 within 90 days of the measure being signed. But the legislation allows for redactions to prevent harm to national security. “I share the Congress’s goal of releasing as much information as possible about the origin” of the coronavirus, Biden said in a statement after the signing, adding, “We need to get to the bottom of covid-19’s origins to help ensure we can better prevent future pandemics.” Other important news​ Insufficient testing of nursing home staff drove waves of coronavirus infections and deaths of elderly residents in 2020, our colleague Christopher Rowland reports, citing a study published Wednesday in the New England Journal of Medicine. The study found that 1.1 million more staff tests per week nationwide would have saved 427 lives each week from November 2020 to mid-January 2021 during the worst time of nursing home outbreaks before vaccines became available. ​ ​

Your questions answered​ Is there any evidence that, with newer variants, the home-detection coronavirus tests are not as reliable as a year ago? In the last couple of months, I’m seeing plenty of folks with classic covid symptoms and onset claiming negative home coronavirus tests (and doctors not testing specifically for RSV, flu, common community-acquired respiratory infections). — Anne, N.C. Antigen tests, which are the main tests used for rapid home detection, continue to identify the most widely circulating variants, according to experts. But antigen tests are generally less sensitive and less likely to pick up early infections compared with molecular tests. The most common of these is the PCR test, which hunts for the coronavirus’s genetic material. Rapid antigen tests, by comparison, look for proteins from the virus. If someone is testing negative on a rapid test and has covid-19 symptoms, it’s possible they don’t have enough virus circulating to test positive or to infect someone. “If you have symptoms suspicious for covid-19, the best practice is to repeat the test in two days and if negative, try again in another two days,” said Albert Ko, an epidemiologist at the Yale School of Public Health and infectious-disease physician. If you have access to a PCR test and that comes back positive, that is a definitive diagnosis for covid-19. At the same time, with most people no longer masking, there is a lot more transmission of respiratory viruses, “so people who test negative for covid-19 may in fact have gotten ill from viruses for which we don’t routinely test,” Ko said. The Food and Drug Administration monitors the performance of coronavirus diagnostic tests and has information on its websiteabout how tests fare in detecting omicron variants. The FDA identifies two tests that are “expected to have reduced performance for the omicron variants.”​ "​

 

[wildcat03]

Well, it finally happened. 3 years (including 1.5 years of preschool for my daughter) and my family finally has its first COVID infection. My husband went to a couple large in person business events last week. I usually am really stressed around them and remind him to do nasal washes for a few days, but I was working a ton and exhausted. Early Sat AM he developed chills and started feeling bad. He got up with the kids (I had worked 'til 2 AM) but woke me to watch them after an hour or so. As he went to lay down in the guest room I shoved a swab at him and then ran it. I'll admit, I was a bit shocked to see it come back positive. We've done SO MANY rapid tests. I had him do a Telehealth visit for paxlovid which he started within 12 hours of symptom onset. He was 85% better within 24 hours. It's now been 48 hours since the kids and I were exposed. I did a rapid on my daughter (school policy) this AM and it was negative. Fingers crossed.

 

[Austina]

Hope you’ll be alright @wildcat03, my DH got Covid in November, and I was with him 24/7 until he was diagnosed, and I was fine.

 

[wildcat03]

Hope you’ll be alright @wildcat03, my DH got Covid in November, and I was with him 24/7 until he was diagnosed, and I was fine.

That’s good to hear. The kids will really be the determining factor. I hadn’t seen him much due to my work schedule. But he had them solo the evening before he got sick and the morning he was ill. They are toddlers so it’s “full contact parenting.” Everybody is fully vaccinated and boosted in September/October.