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Buzzy Lancet long COVID paper under investigation for ‘data errors’
An editorial that accompanied the paper when it was published in January of last year described it as “the first large cohort study with 6-months’ follow-up” of people hospitalized with COVID-19. The article has received plenty of attention since then.
Titled “6-month consequences of COVID-19 in patients discharged from hospital: a cohort study,” the paper has been cited nearly 1,600 times, according to Clarivate’s Web of Science. Altmetric finds references to it in multiple documents from the World Health Organization.
According to the expression of concern, dated November 24, a reader found inconsistencies between the data in the article and a later paper describing the same cohort of patients after a year of follow-up. That discovery sparked an investigation that is still ongoing:
- On Jan 8, 2021, The Lancet published an Article, 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study, by Chaolin Huang and colleagues. 1 On Aug 28, 2021, The Lancet published an Article, 1-year outcomes in hospital survivors with COVID-19: a longitudinal cohort study, by Lixue Huang and colleagues. 2 We received an inquiry from a researcher on data inconsistencies between these two Articles, and we sought an explanation from the corresponding author of the two papers. On Nov 7, 2022, Lancet editors were informed that inconsistencies between the 6-month and the 1-year data were due to “some variables in the dataset used for the 6-month paper were mistakenly disrupted in order”. In view of the extent of these data errors, we now issue an Expression of Concern about the 6-month paper 1 while we investigate further, including further statistical and clinical review of the corrected data. We will update this notice as soon as we have further information.
The corresponding author of both papers, Bin Cao of China’s National Center for Respiratory Medicine and the China-Japan Friendship Hospital in Beijing, has not responded to our request for comment.
A profile of Cao published in Lancet Infectious Diseases last March described him as “a leading researcher in pneumonia and influenza” who “has been instrumental in increasing knowledge about COVID-19.” In addition to the follow-up study of hospitalized COVID patients:
- Cao’s seminal papers during the COVID-19 pandemic include the first report of the clinical characteristics of COVID-19 patients in Wuhan, the description of the risk factors for mortality for adult inpatients, and the results of trials testing the use of antiviral drugs, including lopinavir-ritonavir, to treat COVID-19 in China.
We reached out to The Lancet’s press office and Richard Horton, the journal’s editor-in-chief, and received this statement:
- The Lancet Group treats all communications between editors and authors or readers as confidential. Investigations are continuing, and the Expression of Concern will be updated as soon as we have further information to share. More information about our policies is available here:
This year, The Lancet overtook the New England Journal of Medicine as the medical journal with the highest impact factor, in large part due to the papers it published about COVID-19.
We’ve counted retractions for three of those papers, most notably a paper about the use of the drug hydroxychloroquine that claimed to use medical data from a company called Surgisphere. As Retraction Watch readers may remember, the article was retracted after sleuths questioned if the data were real, and the company would not produce it for review.
This article first appeared on Retraction Watch.
An editorial that accompanied the paper when it was published in January of last year described it as “the first large cohort study with 6-months’ follow-up” of people hospitalized with COVID-19. The article has received plenty of attention since then.
Titled “6-month consequences of COVID-19 in patients discharged from hospital: a cohort study,” the paper has been cited nearly 1,600 times, according to Clarivate’s Web of Science. Altmetric finds references to it in multiple documents from the World Health Organization.
According to the expression of concern, dated November 24, a reader found inconsistencies between the data in the article and a later paper describing the same cohort of patients after a year of follow-up. That discovery sparked an investigation that is still ongoing:
- On Jan 8, 2021, The Lancet published an Article, 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study, by Chaolin Huang and colleagues. 1 On Aug 28, 2021, The Lancet published an Article, 1-year outcomes in hospital survivors with COVID-19: a longitudinal cohort study, by Lixue Huang and colleagues. 2 We received an inquiry from a researcher on data inconsistencies between these two Articles, and we sought an explanation from the corresponding author of the two papers. On Nov 7, 2022, Lancet editors were informed that inconsistencies between the 6-month and the 1-year data were due to “some variables in the dataset used for the 6-month paper were mistakenly disrupted in order”. In view of the extent of these data errors, we now issue an Expression of Concern about the 6-month paper 1 while we investigate further, including further statistical and clinical review of the corrected data. We will update this notice as soon as we have further information.
The corresponding author of both papers, Bin Cao of China’s National Center for Respiratory Medicine and the China-Japan Friendship Hospital in Beijing, has not responded to our request for comment.
A profile of Cao published in Lancet Infectious Diseases last March described him as “a leading researcher in pneumonia and influenza” who “has been instrumental in increasing knowledge about COVID-19.” In addition to the follow-up study of hospitalized COVID patients:
- Cao’s seminal papers during the COVID-19 pandemic include the first report of the clinical characteristics of COVID-19 patients in Wuhan, the description of the risk factors for mortality for adult inpatients, and the results of trials testing the use of antiviral drugs, including lopinavir-ritonavir, to treat COVID-19 in China.
We reached out to The Lancet’s press office and Richard Horton, the journal’s editor-in-chief, and received this statement:
- The Lancet Group treats all communications between editors and authors or readers as confidential. Investigations are continuing, and the Expression of Concern will be updated as soon as we have further information to share. More information about our policies is available here:
This year, The Lancet overtook the New England Journal of Medicine as the medical journal with the highest impact factor, in large part due to the papers it published about COVID-19.
We’ve counted retractions for three of those papers, most notably a paper about the use of the drug hydroxychloroquine that claimed to use medical data from a company called Surgisphere. As Retraction Watch readers may remember, the article was retracted after sleuths questioned if the data were real, and the company would not produce it for review.
This article first appeared on Retraction Watch.
An editorial that accompanied the paper when it was published in January of last year described it as “the first large cohort study with 6-months’ follow-up” of people hospitalized with COVID-19. The article has received plenty of attention since then.
Titled “6-month consequences of COVID-19 in patients discharged from hospital: a cohort study,” the paper has been cited nearly 1,600 times, according to Clarivate’s Web of Science. Altmetric finds references to it in multiple documents from the World Health Organization.
According to the expression of concern, dated November 24, a reader found inconsistencies between the data in the article and a later paper describing the same cohort of patients after a year of follow-up. That discovery sparked an investigation that is still ongoing:
- On Jan 8, 2021, The Lancet published an Article, 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study, by Chaolin Huang and colleagues. 1 On Aug 28, 2021, The Lancet published an Article, 1-year outcomes in hospital survivors with COVID-19: a longitudinal cohort study, by Lixue Huang and colleagues. 2 We received an inquiry from a researcher on data inconsistencies between these two Articles, and we sought an explanation from the corresponding author of the two papers. On Nov 7, 2022, Lancet editors were informed that inconsistencies between the 6-month and the 1-year data were due to “some variables in the dataset used for the 6-month paper were mistakenly disrupted in order”. In view of the extent of these data errors, we now issue an Expression of Concern about the 6-month paper 1 while we investigate further, including further statistical and clinical review of the corrected data. We will update this notice as soon as we have further information.
The corresponding author of both papers, Bin Cao of China’s National Center for Respiratory Medicine and the China-Japan Friendship Hospital in Beijing, has not responded to our request for comment.
A profile of Cao published in Lancet Infectious Diseases last March described him as “a leading researcher in pneumonia and influenza” who “has been instrumental in increasing knowledge about COVID-19.” In addition to the follow-up study of hospitalized COVID patients:
- Cao’s seminal papers during the COVID-19 pandemic include the first report of the clinical characteristics of COVID-19 patients in Wuhan, the description of the risk factors for mortality for adult inpatients, and the results of trials testing the use of antiviral drugs, including lopinavir-ritonavir, to treat COVID-19 in China.
We reached out to The Lancet’s press office and Richard Horton, the journal’s editor-in-chief, and received this statement:
- The Lancet Group treats all communications between editors and authors or readers as confidential. Investigations are continuing, and the Expression of Concern will be updated as soon as we have further information to share. More information about our policies is available here:
This year, The Lancet overtook the New England Journal of Medicine as the medical journal with the highest impact factor, in large part due to the papers it published about COVID-19.
We’ve counted retractions for three of those papers, most notably a paper about the use of the drug hydroxychloroquine that claimed to use medical data from a company called Surgisphere. As Retraction Watch readers may remember, the article was retracted after sleuths questioned if the data were real, and the company would not produce it for review.
This article first appeared on Retraction Watch.
Covid vax prevents death in children regardless of variant
The vaccine’s effectiveness against infection in the short term has been established, as has the waning effectiveness of the vaccine over time, wrote Juan Manuel Castelli, MD, of the Ministry of Health of Argentina, Buenos Aires, and colleagues, in the British Medical Journal.
However, data on the impact of vaccine effectiveness on mortality in children and adolescents are limited, especially during periods of omicron variant dominance, the researchers said.
In their new study, the researchers reviewed data from 844,460 children and adolescents aged 3-17 years from the National Surveillance System and the Nominalized Federal Vaccination Registry of Argentina, during a time that included a period of omicron dominance.
Argentina began vaccinating adolescents aged 12-17 years against COVID-19 in August 2021 and added children aged 3-11 years in October 2021. Those aged 12-17 years who were considered fully vaccinated received two doses of either Pfizer-BioNTech and/or Moderna vaccines, and fully-vaccinated 3- to 11-year-olds received two doses of Sinopharm vaccine.
The average time from the second vaccine dose to a COVID-19 test was 66 days for those aged 12-17 years and 54 days for 3- to 11-year-olds. The researchers matched COVID-19 cases with uninfected controls, and a total of 139,321 cases were included in the analysis.
Overall, the estimated vaccine effectiveness against COVID-19 was 64.2% during a period of delta dominance (61.2% in children aged 3-11 years and 66.8% in adolescents aged 12-17 years).
During a period of omicron dominance, estimated vaccine effectiveness was 19.9% across all ages (15.9% and 26.0% for younger and older age groups, respectively).
Effectiveness of the vaccine decreased over time, regardless of the dominant variant, but the decline was greater during the omicron dominant period, the researchers noted. During the omicron period, effectiveness in children aged 3-11 years decreased from 37.6% at 15-30 days postvaccination to 2.0% at 60 days or longer after vaccination. In adolescents aged 12-17 years, vaccine effectiveness during the omicron period decreased from 55.8% at 15-30 days postvaccination to 12.4% at 60 days or longer after vaccination.
Despite the waning protection against infection, the vaccine’s effectiveness against death from COVID-19 was 66.9% in children aged 3-11 years and 97.6% in adolescents aged 12-17 during the period of omicron dominance, the researchers noted.
The results are consistent with similar studies showing a decreased vaccine effectiveness against infection but a persistent effectiveness against deaths over time, the researchers wrote in the discussion section of their paper.
“Our results suggest that the primary vaccination schedule is effective in preventing mortality in children and adolescents with COVID-19 regardless of the circulating SARS-CoV-2 variant,” the researchers said.
Study limitations and strengths
The study was limited by several factors including the incomplete data on symptoms and hospital admissions, the possible impact of unmeasured confounding variables, and the observational design that prevents conclusions of causality, the researchers noted. However, the results were strengthened by the large sample size and access to detailed vaccination records, they said.
Both heterologous and homologous mRNA vaccine schedules showed similar effectiveness in preventing short-term infection and mortality from COVID-19 during periods of differing dominant variants, they noted.
The study findings support the vaccination of children against COVID-19 as an important public health measure to prevent mortality in children and adolescents, they concluded.
Data support value of vaccination, outside experts say
“COVID vaccines may not be as effective over time as the gene variants in the SARS-CoV-2 virus change,” Adrienne G. Randolph, MD, a pediatrician at Harvard Medical School and Boston Children’s Hospital, said in an interview. “Therefore, it is essential to assess vaccine effectiveness over time to look at effectiveness against variants and duration of effectiveness.” Dr. Randolph, who was not involved in the study, said she was not surprised by the findings, which she described as consistent with data from the United States. “COVID vaccines are very effective against preventing life-threatening disease, but the effectiveness against less severe illness for COVID vaccines is not as effective against Omicron,” she noted.
The take-home message for clinicians is that it’s important to get children vaccinated against COVID to prevent severe and life-threatening illness, said Dr. Randolph. “Although these cases are uncommon in children, it is not possible to predict which children will be the most severely affected by COVID,” she emphasized.
However, “we need more data on the new COVID booster vaccines in children that are designed to be more effective against Omicron’s newer variants,” Dr. Randolph said in an interview. “We also need more data on COVID vaccine effectiveness in the youngest children, under 5 years of age, and data on vaccinating mothers to prevent COVID in infants,” she said.
Tim Joos, MD, a Seattle-based clinician who practices a combination of internal medicine and pediatrics, agreed that future research should continue to assess how the new COVID boosters are faring against new variants, noting that the current study did not include data from children who received the new bivalent vaccine.
“The methodology of this study uses a test negative case control design which is common for estimating vaccine effectiveness post-release of a vaccine, but is subject to biases,” Dr. Joos explained. “These are not the clean effectiveness numbers of the prospective randomized control trials that we are used to hearing about when a vaccine is first being approved.”
“Nevertheless, the study reinforces the initial manufacturers’ studies that the vaccines are effective at preventing infection in the pediatric population,” Dr. Joos said in an interview. The current study also reinforces the effectiveness of vaccines in preventing “the rare but devastating mortality from COVID-19 in the pediatric population.”
Commenting on other research showing an increasing ratio of COVID deaths among vaccinated individuals compared to total COVID deaths, he noted that this finding is “likely reflecting a denominator effect of rapidly declining COVID deaths overall,” partly from the vaccines and partly from immunity after previous natural infection.
The study received no outside funding. The researchers, Dr. Randolph, and Dr. Joos had no financial conflicts to disclose. Dr. Joos serves on the Editorial Advisory Board of Pediatric News.
The vaccine’s effectiveness against infection in the short term has been established, as has the waning effectiveness of the vaccine over time, wrote Juan Manuel Castelli, MD, of the Ministry of Health of Argentina, Buenos Aires, and colleagues, in the British Medical Journal.
However, data on the impact of vaccine effectiveness on mortality in children and adolescents are limited, especially during periods of omicron variant dominance, the researchers said.
In their new study, the researchers reviewed data from 844,460 children and adolescents aged 3-17 years from the National Surveillance System and the Nominalized Federal Vaccination Registry of Argentina, during a time that included a period of omicron dominance.
Argentina began vaccinating adolescents aged 12-17 years against COVID-19 in August 2021 and added children aged 3-11 years in October 2021. Those aged 12-17 years who were considered fully vaccinated received two doses of either Pfizer-BioNTech and/or Moderna vaccines, and fully-vaccinated 3- to 11-year-olds received two doses of Sinopharm vaccine.
The average time from the second vaccine dose to a COVID-19 test was 66 days for those aged 12-17 years and 54 days for 3- to 11-year-olds. The researchers matched COVID-19 cases with uninfected controls, and a total of 139,321 cases were included in the analysis.
Overall, the estimated vaccine effectiveness against COVID-19 was 64.2% during a period of delta dominance (61.2% in children aged 3-11 years and 66.8% in adolescents aged 12-17 years).
During a period of omicron dominance, estimated vaccine effectiveness was 19.9% across all ages (15.9% and 26.0% for younger and older age groups, respectively).
Effectiveness of the vaccine decreased over time, regardless of the dominant variant, but the decline was greater during the omicron dominant period, the researchers noted. During the omicron period, effectiveness in children aged 3-11 years decreased from 37.6% at 15-30 days postvaccination to 2.0% at 60 days or longer after vaccination. In adolescents aged 12-17 years, vaccine effectiveness during the omicron period decreased from 55.8% at 15-30 days postvaccination to 12.4% at 60 days or longer after vaccination.
Despite the waning protection against infection, the vaccine’s effectiveness against death from COVID-19 was 66.9% in children aged 3-11 years and 97.6% in adolescents aged 12-17 during the period of omicron dominance, the researchers noted.
The results are consistent with similar studies showing a decreased vaccine effectiveness against infection but a persistent effectiveness against deaths over time, the researchers wrote in the discussion section of their paper.
“Our results suggest that the primary vaccination schedule is effective in preventing mortality in children and adolescents with COVID-19 regardless of the circulating SARS-CoV-2 variant,” the researchers said.
Study limitations and strengths
The study was limited by several factors including the incomplete data on symptoms and hospital admissions, the possible impact of unmeasured confounding variables, and the observational design that prevents conclusions of causality, the researchers noted. However, the results were strengthened by the large sample size and access to detailed vaccination records, they said.
Both heterologous and homologous mRNA vaccine schedules showed similar effectiveness in preventing short-term infection and mortality from COVID-19 during periods of differing dominant variants, they noted.
The study findings support the vaccination of children against COVID-19 as an important public health measure to prevent mortality in children and adolescents, they concluded.
Data support value of vaccination, outside experts say
“COVID vaccines may not be as effective over time as the gene variants in the SARS-CoV-2 virus change,” Adrienne G. Randolph, MD, a pediatrician at Harvard Medical School and Boston Children’s Hospital, said in an interview. “Therefore, it is essential to assess vaccine effectiveness over time to look at effectiveness against variants and duration of effectiveness.” Dr. Randolph, who was not involved in the study, said she was not surprised by the findings, which she described as consistent with data from the United States. “COVID vaccines are very effective against preventing life-threatening disease, but the effectiveness against less severe illness for COVID vaccines is not as effective against Omicron,” she noted.
The take-home message for clinicians is that it’s important to get children vaccinated against COVID to prevent severe and life-threatening illness, said Dr. Randolph. “Although these cases are uncommon in children, it is not possible to predict which children will be the most severely affected by COVID,” she emphasized.
However, “we need more data on the new COVID booster vaccines in children that are designed to be more effective against Omicron’s newer variants,” Dr. Randolph said in an interview. “We also need more data on COVID vaccine effectiveness in the youngest children, under 5 years of age, and data on vaccinating mothers to prevent COVID in infants,” she said.
Tim Joos, MD, a Seattle-based clinician who practices a combination of internal medicine and pediatrics, agreed that future research should continue to assess how the new COVID boosters are faring against new variants, noting that the current study did not include data from children who received the new bivalent vaccine.
“The methodology of this study uses a test negative case control design which is common for estimating vaccine effectiveness post-release of a vaccine, but is subject to biases,” Dr. Joos explained. “These are not the clean effectiveness numbers of the prospective randomized control trials that we are used to hearing about when a vaccine is first being approved.”
“Nevertheless, the study reinforces the initial manufacturers’ studies that the vaccines are effective at preventing infection in the pediatric population,” Dr. Joos said in an interview. The current study also reinforces the effectiveness of vaccines in preventing “the rare but devastating mortality from COVID-19 in the pediatric population.”
Commenting on other research showing an increasing ratio of COVID deaths among vaccinated individuals compared to total COVID deaths, he noted that this finding is “likely reflecting a denominator effect of rapidly declining COVID deaths overall,” partly from the vaccines and partly from immunity after previous natural infection.
The study received no outside funding. The researchers, Dr. Randolph, and Dr. Joos had no financial conflicts to disclose. Dr. Joos serves on the Editorial Advisory Board of Pediatric News.
The vaccine’s effectiveness against infection in the short term has been established, as has the waning effectiveness of the vaccine over time, wrote Juan Manuel Castelli, MD, of the Ministry of Health of Argentina, Buenos Aires, and colleagues, in the British Medical Journal.
However, data on the impact of vaccine effectiveness on mortality in children and adolescents are limited, especially during periods of omicron variant dominance, the researchers said.
In their new study, the researchers reviewed data from 844,460 children and adolescents aged 3-17 years from the National Surveillance System and the Nominalized Federal Vaccination Registry of Argentina, during a time that included a period of omicron dominance.
Argentina began vaccinating adolescents aged 12-17 years against COVID-19 in August 2021 and added children aged 3-11 years in October 2021. Those aged 12-17 years who were considered fully vaccinated received two doses of either Pfizer-BioNTech and/or Moderna vaccines, and fully-vaccinated 3- to 11-year-olds received two doses of Sinopharm vaccine.
The average time from the second vaccine dose to a COVID-19 test was 66 days for those aged 12-17 years and 54 days for 3- to 11-year-olds. The researchers matched COVID-19 cases with uninfected controls, and a total of 139,321 cases were included in the analysis.
Overall, the estimated vaccine effectiveness against COVID-19 was 64.2% during a period of delta dominance (61.2% in children aged 3-11 years and 66.8% in adolescents aged 12-17 years).
During a period of omicron dominance, estimated vaccine effectiveness was 19.9% across all ages (15.9% and 26.0% for younger and older age groups, respectively).
Effectiveness of the vaccine decreased over time, regardless of the dominant variant, but the decline was greater during the omicron dominant period, the researchers noted. During the omicron period, effectiveness in children aged 3-11 years decreased from 37.6% at 15-30 days postvaccination to 2.0% at 60 days or longer after vaccination. In adolescents aged 12-17 years, vaccine effectiveness during the omicron period decreased from 55.8% at 15-30 days postvaccination to 12.4% at 60 days or longer after vaccination.
Despite the waning protection against infection, the vaccine’s effectiveness against death from COVID-19 was 66.9% in children aged 3-11 years and 97.6% in adolescents aged 12-17 during the period of omicron dominance, the researchers noted.
The results are consistent with similar studies showing a decreased vaccine effectiveness against infection but a persistent effectiveness against deaths over time, the researchers wrote in the discussion section of their paper.
“Our results suggest that the primary vaccination schedule is effective in preventing mortality in children and adolescents with COVID-19 regardless of the circulating SARS-CoV-2 variant,” the researchers said.
Study limitations and strengths
The study was limited by several factors including the incomplete data on symptoms and hospital admissions, the possible impact of unmeasured confounding variables, and the observational design that prevents conclusions of causality, the researchers noted. However, the results were strengthened by the large sample size and access to detailed vaccination records, they said.
Both heterologous and homologous mRNA vaccine schedules showed similar effectiveness in preventing short-term infection and mortality from COVID-19 during periods of differing dominant variants, they noted.
The study findings support the vaccination of children against COVID-19 as an important public health measure to prevent mortality in children and adolescents, they concluded.
Data support value of vaccination, outside experts say
“COVID vaccines may not be as effective over time as the gene variants in the SARS-CoV-2 virus change,” Adrienne G. Randolph, MD, a pediatrician at Harvard Medical School and Boston Children’s Hospital, said in an interview. “Therefore, it is essential to assess vaccine effectiveness over time to look at effectiveness against variants and duration of effectiveness.” Dr. Randolph, who was not involved in the study, said she was not surprised by the findings, which she described as consistent with data from the United States. “COVID vaccines are very effective against preventing life-threatening disease, but the effectiveness against less severe illness for COVID vaccines is not as effective against Omicron,” she noted.
The take-home message for clinicians is that it’s important to get children vaccinated against COVID to prevent severe and life-threatening illness, said Dr. Randolph. “Although these cases are uncommon in children, it is not possible to predict which children will be the most severely affected by COVID,” she emphasized.
However, “we need more data on the new COVID booster vaccines in children that are designed to be more effective against Omicron’s newer variants,” Dr. Randolph said in an interview. “We also need more data on COVID vaccine effectiveness in the youngest children, under 5 years of age, and data on vaccinating mothers to prevent COVID in infants,” she said.
Tim Joos, MD, a Seattle-based clinician who practices a combination of internal medicine and pediatrics, agreed that future research should continue to assess how the new COVID boosters are faring against new variants, noting that the current study did not include data from children who received the new bivalent vaccine.
“The methodology of this study uses a test negative case control design which is common for estimating vaccine effectiveness post-release of a vaccine, but is subject to biases,” Dr. Joos explained. “These are not the clean effectiveness numbers of the prospective randomized control trials that we are used to hearing about when a vaccine is first being approved.”
“Nevertheless, the study reinforces the initial manufacturers’ studies that the vaccines are effective at preventing infection in the pediatric population,” Dr. Joos said in an interview. The current study also reinforces the effectiveness of vaccines in preventing “the rare but devastating mortality from COVID-19 in the pediatric population.”
Commenting on other research showing an increasing ratio of COVID deaths among vaccinated individuals compared to total COVID deaths, he noted that this finding is “likely reflecting a denominator effect of rapidly declining COVID deaths overall,” partly from the vaccines and partly from immunity after previous natural infection.
The study received no outside funding. The researchers, Dr. Randolph, and Dr. Joos had no financial conflicts to disclose. Dr. Joos serves on the Editorial Advisory Board of Pediatric News.
FROM THE BMJ
What is the genetic influence on the severity of COVID-19?
A striking characteristic of COVID-19 is that the severity of clinical outcomes is remarkably variable. Establishing a prognosis for individuals infected with COVID-19 remains a challenge.
Since the start of the COVID-19 pandemic, the heterogeneity of individuals who progress toward severe disease or death, along with the fact that individuals directly exposed to the virus do not necessarily become sick, supports the hypothesis that genetic risk or protective factors are at play.
In an interview with this news organization, Mayana Zatz, PhD, head professor of genetics and coordinator of the Human Genome and Stem Cell Study Center at the University of São Paulo, explained: “The first case that caught my eye was the case of my neighbors, a couple. He presented COVID-19 symptoms, but his wife, who took care of him, had absolutely no symptoms. I thought that it was strange, but we received 3,000 emails from people saying, ‘This happened to me, too.’”
Reports in the media about seven pairs of monozygotic (MZ) twins who died from COVID-19 within days of one another in Brazil also stood out, said the researcher.
, as well as their pathology. Dr. Zatz’s team analyzed the case of a 31-year-old Brazilian MZ twin brother pair who presented simultaneously with severe COVID-19 and the need for oxygen support, despite their age and good health conditions. Curiously, they were admitted and intubated on the same day, but neither of the twins knew about the other’s situation; they found out only when they were extubated.
The study was carried out at the USP with the collaboration of the State University of São Paulo. The authors mapped the genetic profile (by sequencing the genome responsible for coding proteins, or whole-exome sequencing) and the immune cell profile to evaluate innate and adaptive immunity.
The MZ twin brothers shared the same two rare genetic mutations, which may be associated with their increased risk of developing severe COVID-19. However, since these variants were not studied at the protein or functional level, their pathogenicity has yet to be determined. The twins also had [human leukocyte antigen (HLA)] alleles associated with severe COVID-19, which are important candidates for the mechanisms of innate and adaptive immunity and susceptibility to COVID-19 infection and manifestation.
But one particular oddity stood out to the researchers: One of the brothers required longer hospitalization, and only he reported symptoms of long COVID.
In the authors’ eyes, even though the patients shared genetic mutations potentially associated with the risk of developing severe COVID-19, the differences in clinical progression emphasize that, beyond genetic risk factors, continuous exposure to pathogens over a lifetime and other environmental factors mean that each individual’s immune response is unique, even in twins.
“There is no doubt that genetics contribute to the severity of COVID-19, and environmental factors sometimes give us the opportunity to study the disease, too. Such [is the case with] MZ twins who have genetic similarities, even with changes that take place over a lifetime,” José Eduardo Krieger, MD, PhD, professor of molecular medicine at the University of São Paulo Medical School (FMUSP), told this news organization. “Examining MZ twins is a strategy that may help, but, with n = 2, luck really needs to be on your side to get straight to the problem. You need to combine [these findings] with other studies to solve this conundrum,” said Dr. Krieger, who did not take part in the research.
Large cohorts
Genomic and computer resources allow for the study of large sets of data from thousands of individuals. In each of those sets of data, the signal offered by thousands of markers distributed throughout the genome can be studied. This is the possibility offered by various genomic studies of large cohorts of patients with different clinical manifestations.
“Researchers examine thousands of genetic variants throughout the genome from a large sample of individuals and have the chance, for example, to identify genetic variants that are more prevalent in patients who have presented with severe disease than in those who presented with milder disease,” said Dr. Krieger. “These associations highlight a chromosome region in which one or more genes explain, at least in part, the differences observed.”
Genomewide association studies have identified some genetic variants that indicate severity of COVID-19, with potential impact on the virus entering the cell, the immune response, or the development of cytokine storms.
One of these studies, COVID-19 Host Genetics Initiative (COVID-19 HGI), is an international, open-science collaboration for sharing scientific methods and resources with research groups across the world, with the goal of robustly mapping the host genetic determinants of SARS-CoV-2 infection and the severity of the resulting COVID-19 disease. At the start of 2021, the COVID-19 HGI combined genetic data from 49,562 cases and 2 million controls from 46 studies in 19 countries. A total of 853 samples from the BRACOVID study were included in the meta-analysis. The endeavor enabled the identification of 13 genomewide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19.
The BRACOVID study, in which Dr. Krieger participates, aims to identify host genetic factors that determine the severity of COVID-19. It is currently the largest project of its kind in Latin America. An article provides the analysis of the first 5,233 participants in the BRACOVID study, who were recruited in São Paulo. Of these participants, 3,533 had been infected with COVID-19 and hospitalized at either the Heart Institute or the Central Institute of the FMUSP General Hospital. The remaining 1,700 made up the control group, which included health care professionals and members of the general population. The controls were recruited through serology assays or PCR tests for SARS-CoV-2.
The researchers discovered a region of chromosome 1 that could play a role in modulating immune response and that could lead to an increase in the likelihood of hospitalization across a wide range of COVID-19 risk factors. This region of chromosome 1 was observed only in Brazilians with a strong European ancestry; however, this finding had not been mentioned in previous studies, suggesting that it could harbor a risk allele specific to the Brazilian population.
The study also confirmed most, but not all, of the regions recorded in the literature, which may be significant in identifying factors determining severity that are specific to a given population.
Including information from the BRACOVID study, other studies have enhanced the knowledge on affected organs. Combined data from 14,000 patients from nine countries evaluated a region of a single chromosome and found that carriers of a certain allele had a higher probability of experiencing various COVID-19 complications, such as severe respiratory failure, venous thromboembolism, and liver damage. The risk was even higher for individuals aged 60 years and over.
Discordant couples
Smaller sample sizes of underrepresented populations also provide relevant data for genomic studies. Dr. Zatz’s team carried out genomic studies on smaller groups, comparing serodiscordant couples (where one was infected and symptomatic while the partner remained asymptomatic and seronegative despite sharing the same bedroom during the infection). Their research found genetic variants related to immune response that were associated with susceptibility to infection and progression to severe COVID-19.
The team also went on to study a group of patients older than 90 years who recovered from COVID-19 with mild symptoms or who remained asymptomatic following a positive test for SARS-CoV-2. They compared these patients with a sample of elderly patients from the same city (São Paulo), sampled before the current pandemic. The researchers identified a genetic variant related to mucin production. “In individuals with mild COVID-19, the degradation of these mucins would be more efficient,” said Dr. Zatz. It is possible for this variant to interfere not only with the production of mucus, but also in its composition, as there is an exchange of amino acids in the protein.
“We continued the study by comparing the extremes, i.e., those in their 90s with mild COVID-19 and younger patients with severe COVID-19, including several who died,” said Dr. Zatz.
More personalized medicine
The specialists agreed that a genetic test to predict COVID-19 severity is still a long way away. The genetic component is too little understood to enable the evaluation of individual risk. It has been possible to identify several important areas but, as Dr. Krieger pointed out, a variant identified in a certain chromosome interval may not be just one gene. There may be various candidate genes, or there may be a regulatory sequence for a distant gene. Furthermore, there are regions with genes that make sense as moderators of COVID-19 severity, because they regulate an inflammatory or immunologic reaction, but evidence is still lacking.
Reaching the molecular mechanism would, in future, allow a medicine to be chosen for a given patient, as already happens with other diseases. It also could enable the discovery of new medicines following as-yet-unexplored lines of research. Dr. Zatz also considers the possibility of genetic therapy.
Even with the knowledge of human genetics, one part of the equation is missing: viral genetics. “Many of the individuals who were resistant to the Delta variant were later affected by Omicron,” she pointed out.
Significance of Brazil
“We have an infinite amount of genomic data worldwide, but the vast majority originates from White Americans of European origin,” said Dr. Krieger. Moreover, genomic associations of COVID-19 severity discovered in the Chinese population were not significant in the European population. Besides underscoring the importance of collaborating with international studies, this situation supports scientists’ interest in carrying out genetic studies within Brazil, he added.
“In the genomic study of the Brazilian population, we found 2 million variants that were not present in the European populations,” said Dr. Zatz.
Dr. Krieger mentioned a technical advantage that Brazil has. “Having been colonized by different ethnic groups and mixed many generations ago, Brazil has a population with a unique genetic structure; the recombinations are different. When preparing the samples, the regions break differently.” This factor could help to separate, in a candidate region, the gene that is significant from those that might not be.
In general, severe COVID-19 would be a complex phenomenon involving several genes and interactions with environmental factors. The Brazilian studies tried to find a factor that was unique to Brazil, but the significance of the differences remained unclear. “We found some signs that were specific to our population,” concluded Dr. Krieger. “But the reason that more people in Brazil died as a result of COVID-19 was not genetic,” he added.
Dr. Zatz and Dr. Krieger reported no conflicts of interest. This article was translated from the Medscape Portuguese edition.
A version of this article first appeared on Medscape.com.
A striking characteristic of COVID-19 is that the severity of clinical outcomes is remarkably variable. Establishing a prognosis for individuals infected with COVID-19 remains a challenge.
Since the start of the COVID-19 pandemic, the heterogeneity of individuals who progress toward severe disease or death, along with the fact that individuals directly exposed to the virus do not necessarily become sick, supports the hypothesis that genetic risk or protective factors are at play.
In an interview with this news organization, Mayana Zatz, PhD, head professor of genetics and coordinator of the Human Genome and Stem Cell Study Center at the University of São Paulo, explained: “The first case that caught my eye was the case of my neighbors, a couple. He presented COVID-19 symptoms, but his wife, who took care of him, had absolutely no symptoms. I thought that it was strange, but we received 3,000 emails from people saying, ‘This happened to me, too.’”
Reports in the media about seven pairs of monozygotic (MZ) twins who died from COVID-19 within days of one another in Brazil also stood out, said the researcher.
, as well as their pathology. Dr. Zatz’s team analyzed the case of a 31-year-old Brazilian MZ twin brother pair who presented simultaneously with severe COVID-19 and the need for oxygen support, despite their age and good health conditions. Curiously, they were admitted and intubated on the same day, but neither of the twins knew about the other’s situation; they found out only when they were extubated.
The study was carried out at the USP with the collaboration of the State University of São Paulo. The authors mapped the genetic profile (by sequencing the genome responsible for coding proteins, or whole-exome sequencing) and the immune cell profile to evaluate innate and adaptive immunity.
The MZ twin brothers shared the same two rare genetic mutations, which may be associated with their increased risk of developing severe COVID-19. However, since these variants were not studied at the protein or functional level, their pathogenicity has yet to be determined. The twins also had [human leukocyte antigen (HLA)] alleles associated with severe COVID-19, which are important candidates for the mechanisms of innate and adaptive immunity and susceptibility to COVID-19 infection and manifestation.
But one particular oddity stood out to the researchers: One of the brothers required longer hospitalization, and only he reported symptoms of long COVID.
In the authors’ eyes, even though the patients shared genetic mutations potentially associated with the risk of developing severe COVID-19, the differences in clinical progression emphasize that, beyond genetic risk factors, continuous exposure to pathogens over a lifetime and other environmental factors mean that each individual’s immune response is unique, even in twins.
“There is no doubt that genetics contribute to the severity of COVID-19, and environmental factors sometimes give us the opportunity to study the disease, too. Such [is the case with] MZ twins who have genetic similarities, even with changes that take place over a lifetime,” José Eduardo Krieger, MD, PhD, professor of molecular medicine at the University of São Paulo Medical School (FMUSP), told this news organization. “Examining MZ twins is a strategy that may help, but, with n = 2, luck really needs to be on your side to get straight to the problem. You need to combine [these findings] with other studies to solve this conundrum,” said Dr. Krieger, who did not take part in the research.
Large cohorts
Genomic and computer resources allow for the study of large sets of data from thousands of individuals. In each of those sets of data, the signal offered by thousands of markers distributed throughout the genome can be studied. This is the possibility offered by various genomic studies of large cohorts of patients with different clinical manifestations.
“Researchers examine thousands of genetic variants throughout the genome from a large sample of individuals and have the chance, for example, to identify genetic variants that are more prevalent in patients who have presented with severe disease than in those who presented with milder disease,” said Dr. Krieger. “These associations highlight a chromosome region in which one or more genes explain, at least in part, the differences observed.”
Genomewide association studies have identified some genetic variants that indicate severity of COVID-19, with potential impact on the virus entering the cell, the immune response, or the development of cytokine storms.
One of these studies, COVID-19 Host Genetics Initiative (COVID-19 HGI), is an international, open-science collaboration for sharing scientific methods and resources with research groups across the world, with the goal of robustly mapping the host genetic determinants of SARS-CoV-2 infection and the severity of the resulting COVID-19 disease. At the start of 2021, the COVID-19 HGI combined genetic data from 49,562 cases and 2 million controls from 46 studies in 19 countries. A total of 853 samples from the BRACOVID study were included in the meta-analysis. The endeavor enabled the identification of 13 genomewide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19.
The BRACOVID study, in which Dr. Krieger participates, aims to identify host genetic factors that determine the severity of COVID-19. It is currently the largest project of its kind in Latin America. An article provides the analysis of the first 5,233 participants in the BRACOVID study, who were recruited in São Paulo. Of these participants, 3,533 had been infected with COVID-19 and hospitalized at either the Heart Institute or the Central Institute of the FMUSP General Hospital. The remaining 1,700 made up the control group, which included health care professionals and members of the general population. The controls were recruited through serology assays or PCR tests for SARS-CoV-2.
The researchers discovered a region of chromosome 1 that could play a role in modulating immune response and that could lead to an increase in the likelihood of hospitalization across a wide range of COVID-19 risk factors. This region of chromosome 1 was observed only in Brazilians with a strong European ancestry; however, this finding had not been mentioned in previous studies, suggesting that it could harbor a risk allele specific to the Brazilian population.
The study also confirmed most, but not all, of the regions recorded in the literature, which may be significant in identifying factors determining severity that are specific to a given population.
Including information from the BRACOVID study, other studies have enhanced the knowledge on affected organs. Combined data from 14,000 patients from nine countries evaluated a region of a single chromosome and found that carriers of a certain allele had a higher probability of experiencing various COVID-19 complications, such as severe respiratory failure, venous thromboembolism, and liver damage. The risk was even higher for individuals aged 60 years and over.
Discordant couples
Smaller sample sizes of underrepresented populations also provide relevant data for genomic studies. Dr. Zatz’s team carried out genomic studies on smaller groups, comparing serodiscordant couples (where one was infected and symptomatic while the partner remained asymptomatic and seronegative despite sharing the same bedroom during the infection). Their research found genetic variants related to immune response that were associated with susceptibility to infection and progression to severe COVID-19.
The team also went on to study a group of patients older than 90 years who recovered from COVID-19 with mild symptoms or who remained asymptomatic following a positive test for SARS-CoV-2. They compared these patients with a sample of elderly patients from the same city (São Paulo), sampled before the current pandemic. The researchers identified a genetic variant related to mucin production. “In individuals with mild COVID-19, the degradation of these mucins would be more efficient,” said Dr. Zatz. It is possible for this variant to interfere not only with the production of mucus, but also in its composition, as there is an exchange of amino acids in the protein.
“We continued the study by comparing the extremes, i.e., those in their 90s with mild COVID-19 and younger patients with severe COVID-19, including several who died,” said Dr. Zatz.
More personalized medicine
The specialists agreed that a genetic test to predict COVID-19 severity is still a long way away. The genetic component is too little understood to enable the evaluation of individual risk. It has been possible to identify several important areas but, as Dr. Krieger pointed out, a variant identified in a certain chromosome interval may not be just one gene. There may be various candidate genes, or there may be a regulatory sequence for a distant gene. Furthermore, there are regions with genes that make sense as moderators of COVID-19 severity, because they regulate an inflammatory or immunologic reaction, but evidence is still lacking.
Reaching the molecular mechanism would, in future, allow a medicine to be chosen for a given patient, as already happens with other diseases. It also could enable the discovery of new medicines following as-yet-unexplored lines of research. Dr. Zatz also considers the possibility of genetic therapy.
Even with the knowledge of human genetics, one part of the equation is missing: viral genetics. “Many of the individuals who were resistant to the Delta variant were later affected by Omicron,” she pointed out.
Significance of Brazil
“We have an infinite amount of genomic data worldwide, but the vast majority originates from White Americans of European origin,” said Dr. Krieger. Moreover, genomic associations of COVID-19 severity discovered in the Chinese population were not significant in the European population. Besides underscoring the importance of collaborating with international studies, this situation supports scientists’ interest in carrying out genetic studies within Brazil, he added.
“In the genomic study of the Brazilian population, we found 2 million variants that were not present in the European populations,” said Dr. Zatz.
Dr. Krieger mentioned a technical advantage that Brazil has. “Having been colonized by different ethnic groups and mixed many generations ago, Brazil has a population with a unique genetic structure; the recombinations are different. When preparing the samples, the regions break differently.” This factor could help to separate, in a candidate region, the gene that is significant from those that might not be.
In general, severe COVID-19 would be a complex phenomenon involving several genes and interactions with environmental factors. The Brazilian studies tried to find a factor that was unique to Brazil, but the significance of the differences remained unclear. “We found some signs that were specific to our population,” concluded Dr. Krieger. “But the reason that more people in Brazil died as a result of COVID-19 was not genetic,” he added.
Dr. Zatz and Dr. Krieger reported no conflicts of interest. This article was translated from the Medscape Portuguese edition.
A version of this article first appeared on Medscape.com.
A striking characteristic of COVID-19 is that the severity of clinical outcomes is remarkably variable. Establishing a prognosis for individuals infected with COVID-19 remains a challenge.
Since the start of the COVID-19 pandemic, the heterogeneity of individuals who progress toward severe disease or death, along with the fact that individuals directly exposed to the virus do not necessarily become sick, supports the hypothesis that genetic risk or protective factors are at play.
In an interview with this news organization, Mayana Zatz, PhD, head professor of genetics and coordinator of the Human Genome and Stem Cell Study Center at the University of São Paulo, explained: “The first case that caught my eye was the case of my neighbors, a couple. He presented COVID-19 symptoms, but his wife, who took care of him, had absolutely no symptoms. I thought that it was strange, but we received 3,000 emails from people saying, ‘This happened to me, too.’”
Reports in the media about seven pairs of monozygotic (MZ) twins who died from COVID-19 within days of one another in Brazil also stood out, said the researcher.
, as well as their pathology. Dr. Zatz’s team analyzed the case of a 31-year-old Brazilian MZ twin brother pair who presented simultaneously with severe COVID-19 and the need for oxygen support, despite their age and good health conditions. Curiously, they were admitted and intubated on the same day, but neither of the twins knew about the other’s situation; they found out only when they were extubated.
The study was carried out at the USP with the collaboration of the State University of São Paulo. The authors mapped the genetic profile (by sequencing the genome responsible for coding proteins, or whole-exome sequencing) and the immune cell profile to evaluate innate and adaptive immunity.
The MZ twin brothers shared the same two rare genetic mutations, which may be associated with their increased risk of developing severe COVID-19. However, since these variants were not studied at the protein or functional level, their pathogenicity has yet to be determined. The twins also had [human leukocyte antigen (HLA)] alleles associated with severe COVID-19, which are important candidates for the mechanisms of innate and adaptive immunity and susceptibility to COVID-19 infection and manifestation.
But one particular oddity stood out to the researchers: One of the brothers required longer hospitalization, and only he reported symptoms of long COVID.
In the authors’ eyes, even though the patients shared genetic mutations potentially associated with the risk of developing severe COVID-19, the differences in clinical progression emphasize that, beyond genetic risk factors, continuous exposure to pathogens over a lifetime and other environmental factors mean that each individual’s immune response is unique, even in twins.
“There is no doubt that genetics contribute to the severity of COVID-19, and environmental factors sometimes give us the opportunity to study the disease, too. Such [is the case with] MZ twins who have genetic similarities, even with changes that take place over a lifetime,” José Eduardo Krieger, MD, PhD, professor of molecular medicine at the University of São Paulo Medical School (FMUSP), told this news organization. “Examining MZ twins is a strategy that may help, but, with n = 2, luck really needs to be on your side to get straight to the problem. You need to combine [these findings] with other studies to solve this conundrum,” said Dr. Krieger, who did not take part in the research.
Large cohorts
Genomic and computer resources allow for the study of large sets of data from thousands of individuals. In each of those sets of data, the signal offered by thousands of markers distributed throughout the genome can be studied. This is the possibility offered by various genomic studies of large cohorts of patients with different clinical manifestations.
“Researchers examine thousands of genetic variants throughout the genome from a large sample of individuals and have the chance, for example, to identify genetic variants that are more prevalent in patients who have presented with severe disease than in those who presented with milder disease,” said Dr. Krieger. “These associations highlight a chromosome region in which one or more genes explain, at least in part, the differences observed.”
Genomewide association studies have identified some genetic variants that indicate severity of COVID-19, with potential impact on the virus entering the cell, the immune response, or the development of cytokine storms.
One of these studies, COVID-19 Host Genetics Initiative (COVID-19 HGI), is an international, open-science collaboration for sharing scientific methods and resources with research groups across the world, with the goal of robustly mapping the host genetic determinants of SARS-CoV-2 infection and the severity of the resulting COVID-19 disease. At the start of 2021, the COVID-19 HGI combined genetic data from 49,562 cases and 2 million controls from 46 studies in 19 countries. A total of 853 samples from the BRACOVID study were included in the meta-analysis. The endeavor enabled the identification of 13 genomewide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19.
The BRACOVID study, in which Dr. Krieger participates, aims to identify host genetic factors that determine the severity of COVID-19. It is currently the largest project of its kind in Latin America. An article provides the analysis of the first 5,233 participants in the BRACOVID study, who were recruited in São Paulo. Of these participants, 3,533 had been infected with COVID-19 and hospitalized at either the Heart Institute or the Central Institute of the FMUSP General Hospital. The remaining 1,700 made up the control group, which included health care professionals and members of the general population. The controls were recruited through serology assays or PCR tests for SARS-CoV-2.
The researchers discovered a region of chromosome 1 that could play a role in modulating immune response and that could lead to an increase in the likelihood of hospitalization across a wide range of COVID-19 risk factors. This region of chromosome 1 was observed only in Brazilians with a strong European ancestry; however, this finding had not been mentioned in previous studies, suggesting that it could harbor a risk allele specific to the Brazilian population.
The study also confirmed most, but not all, of the regions recorded in the literature, which may be significant in identifying factors determining severity that are specific to a given population.
Including information from the BRACOVID study, other studies have enhanced the knowledge on affected organs. Combined data from 14,000 patients from nine countries evaluated a region of a single chromosome and found that carriers of a certain allele had a higher probability of experiencing various COVID-19 complications, such as severe respiratory failure, venous thromboembolism, and liver damage. The risk was even higher for individuals aged 60 years and over.
Discordant couples
Smaller sample sizes of underrepresented populations also provide relevant data for genomic studies. Dr. Zatz’s team carried out genomic studies on smaller groups, comparing serodiscordant couples (where one was infected and symptomatic while the partner remained asymptomatic and seronegative despite sharing the same bedroom during the infection). Their research found genetic variants related to immune response that were associated with susceptibility to infection and progression to severe COVID-19.
The team also went on to study a group of patients older than 90 years who recovered from COVID-19 with mild symptoms or who remained asymptomatic following a positive test for SARS-CoV-2. They compared these patients with a sample of elderly patients from the same city (São Paulo), sampled before the current pandemic. The researchers identified a genetic variant related to mucin production. “In individuals with mild COVID-19, the degradation of these mucins would be more efficient,” said Dr. Zatz. It is possible for this variant to interfere not only with the production of mucus, but also in its composition, as there is an exchange of amino acids in the protein.
“We continued the study by comparing the extremes, i.e., those in their 90s with mild COVID-19 and younger patients with severe COVID-19, including several who died,” said Dr. Zatz.
More personalized medicine
The specialists agreed that a genetic test to predict COVID-19 severity is still a long way away. The genetic component is too little understood to enable the evaluation of individual risk. It has been possible to identify several important areas but, as Dr. Krieger pointed out, a variant identified in a certain chromosome interval may not be just one gene. There may be various candidate genes, or there may be a regulatory sequence for a distant gene. Furthermore, there are regions with genes that make sense as moderators of COVID-19 severity, because they regulate an inflammatory or immunologic reaction, but evidence is still lacking.
Reaching the molecular mechanism would, in future, allow a medicine to be chosen for a given patient, as already happens with other diseases. It also could enable the discovery of new medicines following as-yet-unexplored lines of research. Dr. Zatz also considers the possibility of genetic therapy.
Even with the knowledge of human genetics, one part of the equation is missing: viral genetics. “Many of the individuals who were resistant to the Delta variant were later affected by Omicron,” she pointed out.
Significance of Brazil
“We have an infinite amount of genomic data worldwide, but the vast majority originates from White Americans of European origin,” said Dr. Krieger. Moreover, genomic associations of COVID-19 severity discovered in the Chinese population were not significant in the European population. Besides underscoring the importance of collaborating with international studies, this situation supports scientists’ interest in carrying out genetic studies within Brazil, he added.
“In the genomic study of the Brazilian population, we found 2 million variants that were not present in the European populations,” said Dr. Zatz.
Dr. Krieger mentioned a technical advantage that Brazil has. “Having been colonized by different ethnic groups and mixed many generations ago, Brazil has a population with a unique genetic structure; the recombinations are different. When preparing the samples, the regions break differently.” This factor could help to separate, in a candidate region, the gene that is significant from those that might not be.
In general, severe COVID-19 would be a complex phenomenon involving several genes and interactions with environmental factors. The Brazilian studies tried to find a factor that was unique to Brazil, but the significance of the differences remained unclear. “We found some signs that were specific to our population,” concluded Dr. Krieger. “But the reason that more people in Brazil died as a result of COVID-19 was not genetic,” he added.
Dr. Zatz and Dr. Krieger reported no conflicts of interest. This article was translated from the Medscape Portuguese edition.
A version of this article first appeared on Medscape.com.
U.S. flu activity already at mid-season levels
according to the Centers of Disease Control and Prevention.
Nationally, 6% of all outpatient visits were because of flu or flu-like illness for the week of Nov. 13-19, up from 5.8% the previous week, the CDC’s Influenza Division said in its weekly FluView report.
Those figures are the highest recorded in November since 2009, but the peak of the 2009-10 flu season occurred even earlier – the week of Oct. 18-24 – and the rate of flu-like illness had already dropped to just over 4.0% by Nov. 15-21 that year and continued to drop thereafter.
Although COVID-19 and respiratory syncytial virus (RSV) are included in the data from the CDC’s Outpatient Influenza-like Illness Surveillance Network, the agency did note that “seasonal influenza activity is elevated across the country” and estimated that “there have been at least 6.2 million illnesses, 53,000 hospitalizations, and 2,900 deaths from flu” during the 2022-23 season.
Total flu deaths include 11 reported in children as of Nov. 19, and children ages 0-4 had a higher proportion of visits for flu like-illness than other age groups.
The agency also said the cumulative hospitalization rate of 11.3 per 100,000 population “is higher than the rate observed in [the corresponding week of] every previous season since 2010-2011.” Adults 65 years and older have the highest cumulative rate, 25.9 per 100,000, for this year, compared with 20.7 for children 0-4; 11.1 for adults 50-64; 10.3 for children 5-17; and 5.6 for adults 18-49 years old, the CDC said.
A version of this article first appeared on WebMD.com.
according to the Centers of Disease Control and Prevention.
Nationally, 6% of all outpatient visits were because of flu or flu-like illness for the week of Nov. 13-19, up from 5.8% the previous week, the CDC’s Influenza Division said in its weekly FluView report.
Those figures are the highest recorded in November since 2009, but the peak of the 2009-10 flu season occurred even earlier – the week of Oct. 18-24 – and the rate of flu-like illness had already dropped to just over 4.0% by Nov. 15-21 that year and continued to drop thereafter.
Although COVID-19 and respiratory syncytial virus (RSV) are included in the data from the CDC’s Outpatient Influenza-like Illness Surveillance Network, the agency did note that “seasonal influenza activity is elevated across the country” and estimated that “there have been at least 6.2 million illnesses, 53,000 hospitalizations, and 2,900 deaths from flu” during the 2022-23 season.
Total flu deaths include 11 reported in children as of Nov. 19, and children ages 0-4 had a higher proportion of visits for flu like-illness than other age groups.
The agency also said the cumulative hospitalization rate of 11.3 per 100,000 population “is higher than the rate observed in [the corresponding week of] every previous season since 2010-2011.” Adults 65 years and older have the highest cumulative rate, 25.9 per 100,000, for this year, compared with 20.7 for children 0-4; 11.1 for adults 50-64; 10.3 for children 5-17; and 5.6 for adults 18-49 years old, the CDC said.
A version of this article first appeared on WebMD.com.
according to the Centers of Disease Control and Prevention.
Nationally, 6% of all outpatient visits were because of flu or flu-like illness for the week of Nov. 13-19, up from 5.8% the previous week, the CDC’s Influenza Division said in its weekly FluView report.
Those figures are the highest recorded in November since 2009, but the peak of the 2009-10 flu season occurred even earlier – the week of Oct. 18-24 – and the rate of flu-like illness had already dropped to just over 4.0% by Nov. 15-21 that year and continued to drop thereafter.
Although COVID-19 and respiratory syncytial virus (RSV) are included in the data from the CDC’s Outpatient Influenza-like Illness Surveillance Network, the agency did note that “seasonal influenza activity is elevated across the country” and estimated that “there have been at least 6.2 million illnesses, 53,000 hospitalizations, and 2,900 deaths from flu” during the 2022-23 season.
Total flu deaths include 11 reported in children as of Nov. 19, and children ages 0-4 had a higher proportion of visits for flu like-illness than other age groups.
The agency also said the cumulative hospitalization rate of 11.3 per 100,000 population “is higher than the rate observed in [the corresponding week of] every previous season since 2010-2011.” Adults 65 years and older have the highest cumulative rate, 25.9 per 100,000, for this year, compared with 20.7 for children 0-4; 11.1 for adults 50-64; 10.3 for children 5-17; and 5.6 for adults 18-49 years old, the CDC said.
A version of this article first appeared on WebMD.com.
More vaccinated people dying of COVID as fewer get booster shots
“We can no longer say this is a pandemic of the unvaccinated,” Kaiser Family Foundation Vice President Cynthia Cox, who conducted the analysis, told The Washington Post.
People who had been vaccinated or boosted made up 58% of COVID-19 deaths in August, the analysis showed. The rate has been on the rise: 23% of coronavirus deaths were among vaccinated people in September 2021, and the vaccinated made up 42% of deaths in January and February 2022, the Post reported.
Research continues to show that people who are vaccinated or boosted have a lower risk of death. The rise in deaths among the vaccinated is the result of three factors, Ms. Cox said.
- A large majority of people in the United States have been vaccinated (267 million people, the said).
- People who are at the greatest risk of dying from COVID-19 are more likely to be vaccinated and boosted, such as the elderly.
- Vaccines lose their effectiveness over time; the virus changes to avoid vaccines; and people need to choose to get boosters to continue to be protected.
The case for the effectiveness of vaccines and boosters versus skipping the shots remains strong. People age 6 months and older who are unvaccinated are six times more likely to die of COVID-19, compared to those who got the primary series of shots, the Post reported. Survival rates were even better with additional booster shots, particularly among older people.
“I feel very confident that if people continue to get vaccinated at good numbers, if people get boosted, we can absolutely have a very safe and healthy holiday season,” Ashish Jha, White House coronavirus czar, said on Nov. 22.
The number of Americans who have gotten the most recent booster has been increasing ahead of the holidays. CDC data show that 12% of the U.S. population age 5 and older has received a booster.
A new study by a team of researchers from Harvard University and Yale University estimates that 94% of the U.S. population has been infected with COVID-19 at least once, leaving just 1 in 20 people who have never had the virus.
“Despite these high exposure numbers, there is still substantial population susceptibility to infection with an Omicron variant,” the authors wrote.
They said that if all states achieved the vaccination levels of Vermont, where 55% of people had at least one booster and 22% got a second one, there would be “an appreciable improvement in population immunity, with greater relative impact for protection against infection versus severe disease. This additional protection results from both the recovery of immunity lost due to waning and the increased effectiveness of the bivalent booster against Omicron infections.”
A version of this article first appeared on WebMD.com.
“We can no longer say this is a pandemic of the unvaccinated,” Kaiser Family Foundation Vice President Cynthia Cox, who conducted the analysis, told The Washington Post.
People who had been vaccinated or boosted made up 58% of COVID-19 deaths in August, the analysis showed. The rate has been on the rise: 23% of coronavirus deaths were among vaccinated people in September 2021, and the vaccinated made up 42% of deaths in January and February 2022, the Post reported.
Research continues to show that people who are vaccinated or boosted have a lower risk of death. The rise in deaths among the vaccinated is the result of three factors, Ms. Cox said.
- A large majority of people in the United States have been vaccinated (267 million people, the said).
- People who are at the greatest risk of dying from COVID-19 are more likely to be vaccinated and boosted, such as the elderly.
- Vaccines lose their effectiveness over time; the virus changes to avoid vaccines; and people need to choose to get boosters to continue to be protected.
The case for the effectiveness of vaccines and boosters versus skipping the shots remains strong. People age 6 months and older who are unvaccinated are six times more likely to die of COVID-19, compared to those who got the primary series of shots, the Post reported. Survival rates were even better with additional booster shots, particularly among older people.
“I feel very confident that if people continue to get vaccinated at good numbers, if people get boosted, we can absolutely have a very safe and healthy holiday season,” Ashish Jha, White House coronavirus czar, said on Nov. 22.
The number of Americans who have gotten the most recent booster has been increasing ahead of the holidays. CDC data show that 12% of the U.S. population age 5 and older has received a booster.
A new study by a team of researchers from Harvard University and Yale University estimates that 94% of the U.S. population has been infected with COVID-19 at least once, leaving just 1 in 20 people who have never had the virus.
“Despite these high exposure numbers, there is still substantial population susceptibility to infection with an Omicron variant,” the authors wrote.
They said that if all states achieved the vaccination levels of Vermont, where 55% of people had at least one booster and 22% got a second one, there would be “an appreciable improvement in population immunity, with greater relative impact for protection against infection versus severe disease. This additional protection results from both the recovery of immunity lost due to waning and the increased effectiveness of the bivalent booster against Omicron infections.”
A version of this article first appeared on WebMD.com.
“We can no longer say this is a pandemic of the unvaccinated,” Kaiser Family Foundation Vice President Cynthia Cox, who conducted the analysis, told The Washington Post.
People who had been vaccinated or boosted made up 58% of COVID-19 deaths in August, the analysis showed. The rate has been on the rise: 23% of coronavirus deaths were among vaccinated people in September 2021, and the vaccinated made up 42% of deaths in January and February 2022, the Post reported.
Research continues to show that people who are vaccinated or boosted have a lower risk of death. The rise in deaths among the vaccinated is the result of three factors, Ms. Cox said.
- A large majority of people in the United States have been vaccinated (267 million people, the said).
- People who are at the greatest risk of dying from COVID-19 are more likely to be vaccinated and boosted, such as the elderly.
- Vaccines lose their effectiveness over time; the virus changes to avoid vaccines; and people need to choose to get boosters to continue to be protected.
The case for the effectiveness of vaccines and boosters versus skipping the shots remains strong. People age 6 months and older who are unvaccinated are six times more likely to die of COVID-19, compared to those who got the primary series of shots, the Post reported. Survival rates were even better with additional booster shots, particularly among older people.
“I feel very confident that if people continue to get vaccinated at good numbers, if people get boosted, we can absolutely have a very safe and healthy holiday season,” Ashish Jha, White House coronavirus czar, said on Nov. 22.
The number of Americans who have gotten the most recent booster has been increasing ahead of the holidays. CDC data show that 12% of the U.S. population age 5 and older has received a booster.
A new study by a team of researchers from Harvard University and Yale University estimates that 94% of the U.S. population has been infected with COVID-19 at least once, leaving just 1 in 20 people who have never had the virus.
“Despite these high exposure numbers, there is still substantial population susceptibility to infection with an Omicron variant,” the authors wrote.
They said that if all states achieved the vaccination levels of Vermont, where 55% of people had at least one booster and 22% got a second one, there would be “an appreciable improvement in population immunity, with greater relative impact for protection against infection versus severe disease. This additional protection results from both the recovery of immunity lost due to waning and the increased effectiveness of the bivalent booster against Omicron infections.”
A version of this article first appeared on WebMD.com.
The right indoor relative humidity could ward off COVID
The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19.
Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.
Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.
The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public.
“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.
The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said.
“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.
Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.
“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”
A version of this article first appeared on WebMD.com.
The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19.
Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.
Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.
The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public.
“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.
The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said.
“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.
Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.
“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”
A version of this article first appeared on WebMD.com.
The “sweet spot” associated with reduced COVID-19 cases and deaths is 40%-60% indoor relative humidity, an MIT news release said. People who maintained indoor relative humidity outside those parameters had higher rates of catching COVID-19.
Most people are comfortable with 30%-50% relative humidity, researchers said. An airplane cabin has about 20% relative humidity.
Relative humidity is the amount of moisture in the air, compared with the total moisture the air can hold at a given temperature before saturating and forming condensation.
The study was published in The Journal of the Royal Society Interface. Researchers examined COVID-19 data and meteorological measurements from 121 countries from January 2020 through August 2020, before vaccines became available to the public.
“When outdoor temperatures were below the typical human comfort range, they assumed indoor spaces were heated to reach that comfort range. Based on the added heating, they calculated the associated drop in indoor relative humidity,” the MIT news release said.
The research teams found that when a region reported a rise in COVID-19 cases and deaths, the region’s estimated indoor relative humidity was either lower than 40% or higher than 60%, the release said.
“There’s potentially a protective effect of this intermediate indoor relative humidity,” said Connor Verheyen, the lead author and a PhD student in medical engineering and medical physics in the Harvard-MIT Program in Health Sciences and Technology.
Widespread use of the 40%-60% indoor humidity range could reduce the need for lockdowns and other widespread restrictions, the study concluded.
“Unlike measures that depend on individual compliance (for example, masking or hand-washing), indoor RH optimization would achieve high compliance because all occupants of a common indoor space would be exposed to similar ambient conditions,” the study said. “Compared to the long timelines and high costs of vaccine production and distribution, humidity control systems could potentially be implemented more quickly and cheaply in certain indoor settings.”
A version of this article first appeared on WebMD.com.
FROM THE JOURNAL OF THE ROYAL SOCIETY INTERFACE
Children and COVID: Weekly cases maintain a low-level plateau
A less-than-1% decrease in weekly COVID-19 cases in children demonstrated continued stability in the pandemic situation as the nation heads into the holiday season.
the American Academy of Pediatrics and the Children’s Hospital Association said in the latest edition of their joint COVID report.
New cases for the week of Nov. 11-17 totaled 27,899, down by 0.9% from the previous week and just 4 weeks removed from the lowest total of the year: 22,719 for Oct. 14-20. There have been just under 15 million cases of COVID-19 in children since the pandemic began, and children represent 18.3% of cases in all ages, the AAP and CHA reported.
Conditions look favorable for that plateau to continue, despite the upcoming holidays, White House COVID-19 coordinator Ashish Jha said recently. “We are in a very different place and we will remain in a different place,” Dr. Jha said, according to STAT News. “We are now at a point where I believe if you’re up to date on your vaccines, you have access to treatments ... there really should be no restrictions on people’s activities.”
One possible spoiler, an apparent spike in COVID-related hospitalizations in children we reported last week, seems to have been a false alarm. The rate of new admissions for Nov. 11, which preliminary data suggested was 0.48 per 100,000 population, has now been revised with more solid data to 0.20 per 100,000, according to the Centers for Disease Control and Prevention.
“We continue to monitor the recent increases in admissions among children. Some of these may be admissions with COVID-19, not because of COVID-19. Co-infections are being noted in our surveillance systems for hospitalizations among children; as much as 10% of admissions or higher have viruses codetected (RSV, influenza, enterovirus/rhinovirus, and other respiratory viruses),” a CDC spokesperson told this news organization.
For children aged 0-17 years, the current 7-day (Nov. 13-19) average number of new admissions with confirmed COVID is 129 per day, down from 147 for the previous 7-day average. Emergency department visits with diagnosed COVID, measured as a percentage of all ED visits, are largely holding steady. The latest 7-day averages available (Nov. 18) – 1.0% for children aged 0-11 years, 0.7% for 12- to 15-year-olds, and 0.8% in 16- to 17-year-olds – are the same or within a tenth of a percent of the rates recorded on Oct. 18, CDC data show.
New vaccinations for the week of Nov. 10-16 were down just slightly for children under age 5 years and for those aged 5-11 years, with a larger drop seen among 12- to 17-year-olds, the AAP said in its weekly vaccination report. So far, 7.9% of all children under age 5 have received at least one dose of COVID vaccine, as have 39.1% of 5 to 11-year-olds and 71.5% of those aged 12-17years, the CDC said on its COVID Data Tracker.
A less-than-1% decrease in weekly COVID-19 cases in children demonstrated continued stability in the pandemic situation as the nation heads into the holiday season.
the American Academy of Pediatrics and the Children’s Hospital Association said in the latest edition of their joint COVID report.
New cases for the week of Nov. 11-17 totaled 27,899, down by 0.9% from the previous week and just 4 weeks removed from the lowest total of the year: 22,719 for Oct. 14-20. There have been just under 15 million cases of COVID-19 in children since the pandemic began, and children represent 18.3% of cases in all ages, the AAP and CHA reported.
Conditions look favorable for that plateau to continue, despite the upcoming holidays, White House COVID-19 coordinator Ashish Jha said recently. “We are in a very different place and we will remain in a different place,” Dr. Jha said, according to STAT News. “We are now at a point where I believe if you’re up to date on your vaccines, you have access to treatments ... there really should be no restrictions on people’s activities.”
One possible spoiler, an apparent spike in COVID-related hospitalizations in children we reported last week, seems to have been a false alarm. The rate of new admissions for Nov. 11, which preliminary data suggested was 0.48 per 100,000 population, has now been revised with more solid data to 0.20 per 100,000, according to the Centers for Disease Control and Prevention.
“We continue to monitor the recent increases in admissions among children. Some of these may be admissions with COVID-19, not because of COVID-19. Co-infections are being noted in our surveillance systems for hospitalizations among children; as much as 10% of admissions or higher have viruses codetected (RSV, influenza, enterovirus/rhinovirus, and other respiratory viruses),” a CDC spokesperson told this news organization.
For children aged 0-17 years, the current 7-day (Nov. 13-19) average number of new admissions with confirmed COVID is 129 per day, down from 147 for the previous 7-day average. Emergency department visits with diagnosed COVID, measured as a percentage of all ED visits, are largely holding steady. The latest 7-day averages available (Nov. 18) – 1.0% for children aged 0-11 years, 0.7% for 12- to 15-year-olds, and 0.8% in 16- to 17-year-olds – are the same or within a tenth of a percent of the rates recorded on Oct. 18, CDC data show.
New vaccinations for the week of Nov. 10-16 were down just slightly for children under age 5 years and for those aged 5-11 years, with a larger drop seen among 12- to 17-year-olds, the AAP said in its weekly vaccination report. So far, 7.9% of all children under age 5 have received at least one dose of COVID vaccine, as have 39.1% of 5 to 11-year-olds and 71.5% of those aged 12-17years, the CDC said on its COVID Data Tracker.
A less-than-1% decrease in weekly COVID-19 cases in children demonstrated continued stability in the pandemic situation as the nation heads into the holiday season.
the American Academy of Pediatrics and the Children’s Hospital Association said in the latest edition of their joint COVID report.
New cases for the week of Nov. 11-17 totaled 27,899, down by 0.9% from the previous week and just 4 weeks removed from the lowest total of the year: 22,719 for Oct. 14-20. There have been just under 15 million cases of COVID-19 in children since the pandemic began, and children represent 18.3% of cases in all ages, the AAP and CHA reported.
Conditions look favorable for that plateau to continue, despite the upcoming holidays, White House COVID-19 coordinator Ashish Jha said recently. “We are in a very different place and we will remain in a different place,” Dr. Jha said, according to STAT News. “We are now at a point where I believe if you’re up to date on your vaccines, you have access to treatments ... there really should be no restrictions on people’s activities.”
One possible spoiler, an apparent spike in COVID-related hospitalizations in children we reported last week, seems to have been a false alarm. The rate of new admissions for Nov. 11, which preliminary data suggested was 0.48 per 100,000 population, has now been revised with more solid data to 0.20 per 100,000, according to the Centers for Disease Control and Prevention.
“We continue to monitor the recent increases in admissions among children. Some of these may be admissions with COVID-19, not because of COVID-19. Co-infections are being noted in our surveillance systems for hospitalizations among children; as much as 10% of admissions or higher have viruses codetected (RSV, influenza, enterovirus/rhinovirus, and other respiratory viruses),” a CDC spokesperson told this news organization.
For children aged 0-17 years, the current 7-day (Nov. 13-19) average number of new admissions with confirmed COVID is 129 per day, down from 147 for the previous 7-day average. Emergency department visits with diagnosed COVID, measured as a percentage of all ED visits, are largely holding steady. The latest 7-day averages available (Nov. 18) – 1.0% for children aged 0-11 years, 0.7% for 12- to 15-year-olds, and 0.8% in 16- to 17-year-olds – are the same or within a tenth of a percent of the rates recorded on Oct. 18, CDC data show.
New vaccinations for the week of Nov. 10-16 were down just slightly for children under age 5 years and for those aged 5-11 years, with a larger drop seen among 12- to 17-year-olds, the AAP said in its weekly vaccination report. So far, 7.9% of all children under age 5 have received at least one dose of COVID vaccine, as have 39.1% of 5 to 11-year-olds and 71.5% of those aged 12-17years, the CDC said on its COVID Data Tracker.
Major life stressors ‘strongly predictive’ of long COVID symptoms
new research suggests.
Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.
These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.
The findings were published online in the Journal of the Neurological Sciences.
Major stressful events common
Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points.
Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.
In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8.
The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.
Long-term sequelae of COVID are increasingly recognized as major public health issues.
It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work.
Holistic approach
Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”
She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”
Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.
She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.
“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.
“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.
The study had no commercial funding. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.
These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.
The findings were published online in the Journal of the Neurological Sciences.
Major stressful events common
Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points.
Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.
In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8.
The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.
Long-term sequelae of COVID are increasingly recognized as major public health issues.
It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work.
Holistic approach
Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”
She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”
Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.
She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.
“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.
“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.
The study had no commercial funding. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
Major life stressors in the year after hospital discharge for COVID-19 are “strongly predictive of a lot of the important outcomes that people may face after COVID,” lead investigator Jennifer A. Frontera, MD, a professor in the department of neurology at New York University Langone Health, said in an interview.
These outcomes include depression, brain fog, fatigue, trouble sleeping, and other long COVID symptoms.
The findings were published online in the Journal of the Neurological Sciences.
Major stressful events common
Dr. Frontera and the NYU Neurology COVID-19 study team evaluated 451 adults who survived a COVID hospital stay. Of these, 383 completed a 6-month follow-up, 242 completed a 12-month follow-up, and 174 completed follow-up at both time points.
Within 1 year of discharge, 77 (17%) patients died and 51% suffered a major stressful life event.
In multivariable analyses, major life stressors – including financial insecurity, food insecurity, death of a close contact, and new disability – were strong independent predictors of disability, trouble with activities of daily living, depression, fatigue, sleep problems, and prolonged post-acute COVID symptoms. The adjusted odds ratios for these outcomes ranged from 2.5 to 20.8.
The research also confirmed the contribution of traditional risk factors for long COVID symptoms, as shown in past studies. These include older age, poor pre-COVID functional status, and more severe initial COVID-19 infection.
Long-term sequelae of COVID are increasingly recognized as major public health issues.
It has been estimated that roughly 16 million U.S. adults aged 18-65 years ave long COVID, with the often debilitating symptoms keeping up to 4 million out of work.
Holistic approach
Dr. Frontera said it’s important to realize that “sleep, fatigue, anxiety, depression, even cognition are so interwoven with each other that anything that impacts any one of them could have repercussions on the other.”
She added that it “certainly makes sense that there is an interplay or even a bidirectional relationship between the stressors that people face and how well they can recover after COVID.”
Therapies that lessen the trauma of the most stress-inducing life events need to be a central part of treatment for long COVID, with more research needed to validate the best approaches, Dr. Frontera said.
She also noted that social services or case management resources may be able to help address at least some of the stressors that individuals are under – and it is important to refer them to these resources. Referral to mental health services is also important.
“I think it’s really important to take a holistic approach and try to deal with whatever the problem may be,” said Dr. Frontera.
“I’m a neurologist, but as part of my evaluation, I really need to address if there are life stressors or mental health issues that may be impacting this person’s function,” she added.
The study had no commercial funding. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE NEUROLOGICAL SCIENCES
Experts explain the ‘perfect storm’ of rampant RSV and flu
Headlines over the past few weeks are ringing the alarm about earlier and more serious influenza (flu) and respiratory syncytial virus (RSV) outbreaks compared with previous years. Add COVID-19 to the mix and you have a dangerous mash of viruses that have many experts calling for caution and searching for explanations.
RSV and the flu “are certainly getting more attention, and they’re getting more attention for two reasons,” said William Schaffner, MD, professor of preventive medicine and infectious diseases at Vanderbilt University, Nashville, Tenn.
“The first is that they’re both extraordinarily early. The second is that they’re both out there spreading very, very rapidly,” he told this news organization.
RSV usually follows a seasonal pattern with cases peaking in January and February. Both viruses tend to hit different regions of the country at different times, and that’s not the case in 2022.
“This is particularly striking for RSV, which usually doesn’t affect the entire country simultaneously,” Dr. Schaffner said.
“Yes, RSV is causing many more hospitalizations and earlier than any previously recorded season in the U.S.,” according to figures from the Centers for Disease Control and Prevention on RSV hospitalizations, said Kevin Messacar, MD, PhD, associate professor at the University of Colorado at Denver, Aurora, and a pediatric infectious disease specialist at Children’s Hospital Colorado in Aurora.
Although there could be some increase in diagnoses because of increased awareness, the jump in RSV and flu cases “is a real phenomenon for multiple reasons,” said Peter Chin-Hong, MD, professor in the division of infectious diseases at the University of California, San Francisco.
With fewer COVID-related restrictions, people are moving around more. Also, during fall and winter, people tend to gather indoors. Colder temperatures and lower humidity contribute as well, Dr. Chin-Hong said, because “the droplets are just simply lighter.
“I think those are all factors,” he told this news organization.
Paul Auwaerter, MD, agreed that there are likely multiple causes for the unusual timing and severity of RSV and flu this year.
“Change in behaviors is a leading cause,” said the clinical director for the division of infectious diseases at the Johns Hopkins University, Baltimore. More people returning to the workplace and children going to school without masks are examples, he added.
Less exposure to these three viruses also means there was less immune boosting among existing populations, he said. This can lead to “larger susceptible populations, especially infants and younger children, due to the relative absence of circulating virus in past years.”
A leading theory
Are we paying a price now for people following the edicts from officials to mask up, stand apart, and take other personal and public health precautions during the COVID-19 pandemic?
It’s possible, but that may not be the whole story.
“When it comes to RSV, I think that theory of isolation, social distancing, mask wearing, and not attending schools is a very valid one,” Dr. Schaffner said. “That’s everybody’s favorite [reason].”
He said he is confident that the jump in RSV cases is being driven by previous COVID public health protections. However, he’s “a little more cautious about influenza, in part because influenza is so variable.
“Like people in influenza say, if you’ve seen one influenza season, you’ve seen one influenza season,” Dr. Schaffner said.
“There’s a lot of debate,” he added. “Nobody can say definitively whether the immune deficit or debt is a consequence of not being stimulated and restimulated by the influenza virus over the past two seasons.”
‘A perfect storm’
“Now you kind of have the perfect storm,” Dr. Chin-Hong said. “It’s not a good situation for COVID with the variants that are emerging. For influenza, not having seen a lot of influenza the last 2 years, we’re probably more susceptible to getting infected.”
RSV cases rose during summer 2021, but now the weather is colder, and people are interacting more closely. “And it’s very, very transmissible,” he said.
Dr. Chin-Hong also predicted that “even though we don’t have a lot of COVID now, COVID will probably pick up.”
The rise in RSV was unexpected by some experts. “This early influenza is also a bit of a surprise and may be influenced by the fact that lots of us are going back and seeing each other again close-to-close, face-to-face in many enclosed environments,” Dr. Schaffner said.
He estimated the 2022-2023 flu season started 4-6 weeks early “and it’s taken off like a rocket. It started in the Southeast, quickly went to the Southwest and up the East Coast. Now it’s moving dramatically through the Midwest and will continue. It’s quite sure to hit the West Coast if it isn’t there already.”
A phenomenon by any other name
Some are calling the situation an “immunity debt,” while others dub it an “immunity pause” or an “immunity deficit.” Many physicians and immunologists have taken to social media to push back on the term “immunity debt,” saying it’s a mischaracterization that is being used to vilify COVID precautions, such as masking, social distancing, and other protective measures taken during the pandemic.
“I prefer the term ‘immunity gap’ ... which is more established in the epidemiology literature, especially given the politicization of the term ‘immunity debt’ by folks recently,” Dr. Messacar said.
“To me, the immunity gap is a scientific observation, not a political argument,” he added.
In a July 2022 publication in The Lancet, Dr. Messacar and his colleagues stated that “decreased exposure to endemic viruses created an immunity gap – a group of susceptible individuals who avoided infection and therefore lack pathogen-specific immunity to protect against future infection. Decreases in childhood vaccinations with pandemic disruptions to health care delivery contribute to this immunity gap for vaccine-preventable diseases, such as influenza,measles, and polio.”
The researchers noted that because of isolation during the pandemic, older children and newborns are being exposed to RSV for the first time. Returning to birthday parties, playing with friends, and going to school without masks means “children are being exposed to RSV, and that’s likely the reason that RSV is moving early and very, very substantially through this now expanded pool of susceptible children,” Dr. Schaffner said.
How likely are coinfections?
With peaks in RSV, flu, and COVID-19 cases each predicted in the coming months, how likely is it that someone could get sick with more than one infection at the same time?
Early in the pandemic, coinfection with COVID and the flu was reported in people at some centers on the West Coast, Dr. Auwaerter said. Now, however, “the unpredictable nature of the Omicron subvariants and the potential for further change, along with the never-before-seen significant lessening of influenza over 2 years, leave little for predictability.
“I do think it is less likely, given the extent of immunity now to SARS-CoV-2 in the population,” Dr. Auwaerter said.
“I most worry about viral coinfections ... in people with suppressed immune systems if we have high community rates of the SARS-CoV-2 and influenza circulating this fall and winter,” he added.
Studies during the pandemic suggest that coinfection with the SARS-CoV-2 virus and another respiratory virus were either rare or nonexistent.
Dr. Schaffner said these findings align with his experience at Vanderbilt University, which is part of a CDC-sponsored network that tracks laboratory-confirmed RSV, flu, and COVID cases among people in the hospital. “Coinfections are, at least to date, very unusual.”
There needs to be an asterisk next to that, Dr. Schaffner added. “Looking back over the last 2 years, we’ve had very little influenza, and we’ve had curtailed RSV seasons. So there hasn’t been a whole lot of opportunity for dual infections to occur.
“So this year may be more revelatory as we go forward,” he said.
Future concerns
The future is uncertain, Dr. Messacar and colleagues wrote in The Lancet: “Crucially, the patterns of these returning viral outbreaks have been heterogeneous across locations, populations, and pathogens, making predictions and preparations challenging.”
Dr. Chin-Hong used a horse race analogy to illustrate the situation now and going forward. RSV is the front-running horse, and influenza is running behind but trying to catch up. “And then COVID is the dark horse. It’s trailing the race right now – but all these variants are giving the horse extra supplements.
“And the COVID horse is probably going to be very competitive with the front-runner,” he said.
“We’re just at the beginning of the race right now,” Dr. Chin-Hong said, “so that’s why we’re worried that these three [viruses] will be even more pronounced come later in the year.”
A version of this article first appeared on Medscape.com.
Headlines over the past few weeks are ringing the alarm about earlier and more serious influenza (flu) and respiratory syncytial virus (RSV) outbreaks compared with previous years. Add COVID-19 to the mix and you have a dangerous mash of viruses that have many experts calling for caution and searching for explanations.
RSV and the flu “are certainly getting more attention, and they’re getting more attention for two reasons,” said William Schaffner, MD, professor of preventive medicine and infectious diseases at Vanderbilt University, Nashville, Tenn.
“The first is that they’re both extraordinarily early. The second is that they’re both out there spreading very, very rapidly,” he told this news organization.
RSV usually follows a seasonal pattern with cases peaking in January and February. Both viruses tend to hit different regions of the country at different times, and that’s not the case in 2022.
“This is particularly striking for RSV, which usually doesn’t affect the entire country simultaneously,” Dr. Schaffner said.
“Yes, RSV is causing many more hospitalizations and earlier than any previously recorded season in the U.S.,” according to figures from the Centers for Disease Control and Prevention on RSV hospitalizations, said Kevin Messacar, MD, PhD, associate professor at the University of Colorado at Denver, Aurora, and a pediatric infectious disease specialist at Children’s Hospital Colorado in Aurora.
Although there could be some increase in diagnoses because of increased awareness, the jump in RSV and flu cases “is a real phenomenon for multiple reasons,” said Peter Chin-Hong, MD, professor in the division of infectious diseases at the University of California, San Francisco.
With fewer COVID-related restrictions, people are moving around more. Also, during fall and winter, people tend to gather indoors. Colder temperatures and lower humidity contribute as well, Dr. Chin-Hong said, because “the droplets are just simply lighter.
“I think those are all factors,” he told this news organization.
Paul Auwaerter, MD, agreed that there are likely multiple causes for the unusual timing and severity of RSV and flu this year.
“Change in behaviors is a leading cause,” said the clinical director for the division of infectious diseases at the Johns Hopkins University, Baltimore. More people returning to the workplace and children going to school without masks are examples, he added.
Less exposure to these three viruses also means there was less immune boosting among existing populations, he said. This can lead to “larger susceptible populations, especially infants and younger children, due to the relative absence of circulating virus in past years.”
A leading theory
Are we paying a price now for people following the edicts from officials to mask up, stand apart, and take other personal and public health precautions during the COVID-19 pandemic?
It’s possible, but that may not be the whole story.
“When it comes to RSV, I think that theory of isolation, social distancing, mask wearing, and not attending schools is a very valid one,” Dr. Schaffner said. “That’s everybody’s favorite [reason].”
He said he is confident that the jump in RSV cases is being driven by previous COVID public health protections. However, he’s “a little more cautious about influenza, in part because influenza is so variable.
“Like people in influenza say, if you’ve seen one influenza season, you’ve seen one influenza season,” Dr. Schaffner said.
“There’s a lot of debate,” he added. “Nobody can say definitively whether the immune deficit or debt is a consequence of not being stimulated and restimulated by the influenza virus over the past two seasons.”
‘A perfect storm’
“Now you kind of have the perfect storm,” Dr. Chin-Hong said. “It’s not a good situation for COVID with the variants that are emerging. For influenza, not having seen a lot of influenza the last 2 years, we’re probably more susceptible to getting infected.”
RSV cases rose during summer 2021, but now the weather is colder, and people are interacting more closely. “And it’s very, very transmissible,” he said.
Dr. Chin-Hong also predicted that “even though we don’t have a lot of COVID now, COVID will probably pick up.”
The rise in RSV was unexpected by some experts. “This early influenza is also a bit of a surprise and may be influenced by the fact that lots of us are going back and seeing each other again close-to-close, face-to-face in many enclosed environments,” Dr. Schaffner said.
He estimated the 2022-2023 flu season started 4-6 weeks early “and it’s taken off like a rocket. It started in the Southeast, quickly went to the Southwest and up the East Coast. Now it’s moving dramatically through the Midwest and will continue. It’s quite sure to hit the West Coast if it isn’t there already.”
A phenomenon by any other name
Some are calling the situation an “immunity debt,” while others dub it an “immunity pause” or an “immunity deficit.” Many physicians and immunologists have taken to social media to push back on the term “immunity debt,” saying it’s a mischaracterization that is being used to vilify COVID precautions, such as masking, social distancing, and other protective measures taken during the pandemic.
“I prefer the term ‘immunity gap’ ... which is more established in the epidemiology literature, especially given the politicization of the term ‘immunity debt’ by folks recently,” Dr. Messacar said.
“To me, the immunity gap is a scientific observation, not a political argument,” he added.
In a July 2022 publication in The Lancet, Dr. Messacar and his colleagues stated that “decreased exposure to endemic viruses created an immunity gap – a group of susceptible individuals who avoided infection and therefore lack pathogen-specific immunity to protect against future infection. Decreases in childhood vaccinations with pandemic disruptions to health care delivery contribute to this immunity gap for vaccine-preventable diseases, such as influenza,measles, and polio.”
The researchers noted that because of isolation during the pandemic, older children and newborns are being exposed to RSV for the first time. Returning to birthday parties, playing with friends, and going to school without masks means “children are being exposed to RSV, and that’s likely the reason that RSV is moving early and very, very substantially through this now expanded pool of susceptible children,” Dr. Schaffner said.
How likely are coinfections?
With peaks in RSV, flu, and COVID-19 cases each predicted in the coming months, how likely is it that someone could get sick with more than one infection at the same time?
Early in the pandemic, coinfection with COVID and the flu was reported in people at some centers on the West Coast, Dr. Auwaerter said. Now, however, “the unpredictable nature of the Omicron subvariants and the potential for further change, along with the never-before-seen significant lessening of influenza over 2 years, leave little for predictability.
“I do think it is less likely, given the extent of immunity now to SARS-CoV-2 in the population,” Dr. Auwaerter said.
“I most worry about viral coinfections ... in people with suppressed immune systems if we have high community rates of the SARS-CoV-2 and influenza circulating this fall and winter,” he added.
Studies during the pandemic suggest that coinfection with the SARS-CoV-2 virus and another respiratory virus were either rare or nonexistent.
Dr. Schaffner said these findings align with his experience at Vanderbilt University, which is part of a CDC-sponsored network that tracks laboratory-confirmed RSV, flu, and COVID cases among people in the hospital. “Coinfections are, at least to date, very unusual.”
There needs to be an asterisk next to that, Dr. Schaffner added. “Looking back over the last 2 years, we’ve had very little influenza, and we’ve had curtailed RSV seasons. So there hasn’t been a whole lot of opportunity for dual infections to occur.
“So this year may be more revelatory as we go forward,” he said.
Future concerns
The future is uncertain, Dr. Messacar and colleagues wrote in The Lancet: “Crucially, the patterns of these returning viral outbreaks have been heterogeneous across locations, populations, and pathogens, making predictions and preparations challenging.”
Dr. Chin-Hong used a horse race analogy to illustrate the situation now and going forward. RSV is the front-running horse, and influenza is running behind but trying to catch up. “And then COVID is the dark horse. It’s trailing the race right now – but all these variants are giving the horse extra supplements.
“And the COVID horse is probably going to be very competitive with the front-runner,” he said.
“We’re just at the beginning of the race right now,” Dr. Chin-Hong said, “so that’s why we’re worried that these three [viruses] will be even more pronounced come later in the year.”
A version of this article first appeared on Medscape.com.
Headlines over the past few weeks are ringing the alarm about earlier and more serious influenza (flu) and respiratory syncytial virus (RSV) outbreaks compared with previous years. Add COVID-19 to the mix and you have a dangerous mash of viruses that have many experts calling for caution and searching for explanations.
RSV and the flu “are certainly getting more attention, and they’re getting more attention for two reasons,” said William Schaffner, MD, professor of preventive medicine and infectious diseases at Vanderbilt University, Nashville, Tenn.
“The first is that they’re both extraordinarily early. The second is that they’re both out there spreading very, very rapidly,” he told this news organization.
RSV usually follows a seasonal pattern with cases peaking in January and February. Both viruses tend to hit different regions of the country at different times, and that’s not the case in 2022.
“This is particularly striking for RSV, which usually doesn’t affect the entire country simultaneously,” Dr. Schaffner said.
“Yes, RSV is causing many more hospitalizations and earlier than any previously recorded season in the U.S.,” according to figures from the Centers for Disease Control and Prevention on RSV hospitalizations, said Kevin Messacar, MD, PhD, associate professor at the University of Colorado at Denver, Aurora, and a pediatric infectious disease specialist at Children’s Hospital Colorado in Aurora.
Although there could be some increase in diagnoses because of increased awareness, the jump in RSV and flu cases “is a real phenomenon for multiple reasons,” said Peter Chin-Hong, MD, professor in the division of infectious diseases at the University of California, San Francisco.
With fewer COVID-related restrictions, people are moving around more. Also, during fall and winter, people tend to gather indoors. Colder temperatures and lower humidity contribute as well, Dr. Chin-Hong said, because “the droplets are just simply lighter.
“I think those are all factors,” he told this news organization.
Paul Auwaerter, MD, agreed that there are likely multiple causes for the unusual timing and severity of RSV and flu this year.
“Change in behaviors is a leading cause,” said the clinical director for the division of infectious diseases at the Johns Hopkins University, Baltimore. More people returning to the workplace and children going to school without masks are examples, he added.
Less exposure to these three viruses also means there was less immune boosting among existing populations, he said. This can lead to “larger susceptible populations, especially infants and younger children, due to the relative absence of circulating virus in past years.”
A leading theory
Are we paying a price now for people following the edicts from officials to mask up, stand apart, and take other personal and public health precautions during the COVID-19 pandemic?
It’s possible, but that may not be the whole story.
“When it comes to RSV, I think that theory of isolation, social distancing, mask wearing, and not attending schools is a very valid one,” Dr. Schaffner said. “That’s everybody’s favorite [reason].”
He said he is confident that the jump in RSV cases is being driven by previous COVID public health protections. However, he’s “a little more cautious about influenza, in part because influenza is so variable.
“Like people in influenza say, if you’ve seen one influenza season, you’ve seen one influenza season,” Dr. Schaffner said.
“There’s a lot of debate,” he added. “Nobody can say definitively whether the immune deficit or debt is a consequence of not being stimulated and restimulated by the influenza virus over the past two seasons.”
‘A perfect storm’
“Now you kind of have the perfect storm,” Dr. Chin-Hong said. “It’s not a good situation for COVID with the variants that are emerging. For influenza, not having seen a lot of influenza the last 2 years, we’re probably more susceptible to getting infected.”
RSV cases rose during summer 2021, but now the weather is colder, and people are interacting more closely. “And it’s very, very transmissible,” he said.
Dr. Chin-Hong also predicted that “even though we don’t have a lot of COVID now, COVID will probably pick up.”
The rise in RSV was unexpected by some experts. “This early influenza is also a bit of a surprise and may be influenced by the fact that lots of us are going back and seeing each other again close-to-close, face-to-face in many enclosed environments,” Dr. Schaffner said.
He estimated the 2022-2023 flu season started 4-6 weeks early “and it’s taken off like a rocket. It started in the Southeast, quickly went to the Southwest and up the East Coast. Now it’s moving dramatically through the Midwest and will continue. It’s quite sure to hit the West Coast if it isn’t there already.”
A phenomenon by any other name
Some are calling the situation an “immunity debt,” while others dub it an “immunity pause” or an “immunity deficit.” Many physicians and immunologists have taken to social media to push back on the term “immunity debt,” saying it’s a mischaracterization that is being used to vilify COVID precautions, such as masking, social distancing, and other protective measures taken during the pandemic.
“I prefer the term ‘immunity gap’ ... which is more established in the epidemiology literature, especially given the politicization of the term ‘immunity debt’ by folks recently,” Dr. Messacar said.
“To me, the immunity gap is a scientific observation, not a political argument,” he added.
In a July 2022 publication in The Lancet, Dr. Messacar and his colleagues stated that “decreased exposure to endemic viruses created an immunity gap – a group of susceptible individuals who avoided infection and therefore lack pathogen-specific immunity to protect against future infection. Decreases in childhood vaccinations with pandemic disruptions to health care delivery contribute to this immunity gap for vaccine-preventable diseases, such as influenza,measles, and polio.”
The researchers noted that because of isolation during the pandemic, older children and newborns are being exposed to RSV for the first time. Returning to birthday parties, playing with friends, and going to school without masks means “children are being exposed to RSV, and that’s likely the reason that RSV is moving early and very, very substantially through this now expanded pool of susceptible children,” Dr. Schaffner said.
How likely are coinfections?
With peaks in RSV, flu, and COVID-19 cases each predicted in the coming months, how likely is it that someone could get sick with more than one infection at the same time?
Early in the pandemic, coinfection with COVID and the flu was reported in people at some centers on the West Coast, Dr. Auwaerter said. Now, however, “the unpredictable nature of the Omicron subvariants and the potential for further change, along with the never-before-seen significant lessening of influenza over 2 years, leave little for predictability.
“I do think it is less likely, given the extent of immunity now to SARS-CoV-2 in the population,” Dr. Auwaerter said.
“I most worry about viral coinfections ... in people with suppressed immune systems if we have high community rates of the SARS-CoV-2 and influenza circulating this fall and winter,” he added.
Studies during the pandemic suggest that coinfection with the SARS-CoV-2 virus and another respiratory virus were either rare or nonexistent.
Dr. Schaffner said these findings align with his experience at Vanderbilt University, which is part of a CDC-sponsored network that tracks laboratory-confirmed RSV, flu, and COVID cases among people in the hospital. “Coinfections are, at least to date, very unusual.”
There needs to be an asterisk next to that, Dr. Schaffner added. “Looking back over the last 2 years, we’ve had very little influenza, and we’ve had curtailed RSV seasons. So there hasn’t been a whole lot of opportunity for dual infections to occur.
“So this year may be more revelatory as we go forward,” he said.
Future concerns
The future is uncertain, Dr. Messacar and colleagues wrote in The Lancet: “Crucially, the patterns of these returning viral outbreaks have been heterogeneous across locations, populations, and pathogens, making predictions and preparations challenging.”
Dr. Chin-Hong used a horse race analogy to illustrate the situation now and going forward. RSV is the front-running horse, and influenza is running behind but trying to catch up. “And then COVID is the dark horse. It’s trailing the race right now – but all these variants are giving the horse extra supplements.
“And the COVID horse is probably going to be very competitive with the front-runner,” he said.
“We’re just at the beginning of the race right now,” Dr. Chin-Hong said, “so that’s why we’re worried that these three [viruses] will be even more pronounced come later in the year.”
A version of this article first appeared on Medscape.com.
Hypertension linked to risk of severe COVID
U.K. researchers have established that hypertension is associated with a 22% greater risk of severe COVID-19, with the odds of severe COVID-19 unaffected by medication type.
Hypertension “appears to be one of the commonest comorbidities in COVID-19 patients”, explained the authors of a new study, published in PLOS ONE. The authors highlighted that previous research had shown that hypertension was more prevalent in severe and fatal cases compared with all cases of COVID-19.
They pointed out, however, that whether hypertensive individuals have a higher risk of severe COVID-19, compared with nonhypertensives, and whether the absolute level of systolic blood pressure or the type of antihypertensive medication is related to this risk, remained “unclear.”
To try to answer these questions, the research team, led by University of Cambridge researchers, analyzed data from 16,134 individuals who tested positive for COVID-19 (mean age 65.3 years, 47% male, 90% white), 40% were diagnosed with essential hypertension at the analysis baseline – 22% of whom had developed severe COVID-19.
Systolic blood pressure (SBP) was categorized by 10–mm Hg ranges, starting from < 120 mm Hg up to 180+ mm Hg, with the reference category defined as 120-129 mm Hg, based on data from the SPRINT study, which demonstrated that intensive SBP lowering to below 120 mm Hg, as compared with the traditional threshold of 140 mm Hg, was beneficial. Diastolic blood pressure was categorized by 10–mm Hg ranges, starting from < 60 mm Hg up to 100+ mm Hg with 80-90 mm Hg being the reference category.
In their analyses the researchers adjusted for age, sex, body mass index, ethnicity, smoking status, diabetes status, socioeconomic status, and inflammation (C-reactive protein [CRP]), as these were proposed as potential confounders. To assess the direct effect of hypertension on COVID-19, they also adjusted for intermediate variables, including cardiovascular comorbidities and stroke, on the causal pathway between hypertension and severe COVID-19.
Majority of effect of hypertension on severe COVID-19 was direct
The unadjusted odds ratio of the association between hypertension and severe COVID-19 was 2.33 (95% confidence interval, 2.16-2.51), the authors emphasized. They found that, after adjusting for all confounding variables, hypertension was associated with 22% higher odds of severe COVID-19 (OR, 1.22; 95% CI, 1.12-1.33), compared with normotension.
Individuals with severe COVID-19 were marginally older, more likely to be male, and more deprived, the authors said. “They were also more likely to be hypertensive, compared with individuals without severe COVID-19, and a greater proportion of individuals with severe COVID-19 had cardiovascular comorbidities.”
The majority of the effect of hypertension on development of severe COVID-19 was “direct,” they said. However, a modest proportion of the effect was mediated via cardiovascular comorbidities such as peripheral vascular disease, MI, coronary heart disease, arrhythmias, and stroke. Of note, those with a history of stroke had a 47% higher risk of severe COVID-19 and those with a history of other cardiovascular comorbidities had a 30% higher risk of severe COVID-19, the authors commented.
J-shaped relationship
Of the total of 6,517 (40%) individuals who had a diagnosis of essential hypertension at baseline, 67% were treated (41% with monotherapy, 59% with combination therapy), and 33% were untreated.
There were similar numbers of severe COVID-19 in each medication group: ACE inhibitors, 34%; angiotensin receptor blockers (ARBs), 36%; and “other” medications 34%.
In hypertensive individuals receiving antihypertensive medications, there was a “J-shaped relationship” between the level of blood pressure and risk of severe COVID-19 when using a systolic blood pressure level of 120-129 mm Hg as a reference – 150-159 mm Hg versus 120-129 mm Hg (OR 1.91; 95% CI, 1.44-2.53), > 180+ mm Hg versus 120-129 mm Hg (OR 1.93; 95% CI, 1.06-3.51).
The authors commented that there was no evidence of a higher risk of severe COVID-19 until systolic blood pressure “exceeded 150 mm Hg.”
They said it was an interesting finding that “very well-controlled” systolic blood pressure < 120 mm Hg was associated with a 40% (OR, 1.40; 95% CI, 1.11-1.78) greater odds of severe COVID-19. “This may be due to reverse causality, where low systolic blood pressure levels may indicate poorer health, such that the occurrence of severe COVID-19 may be related to underlying disease rather than the level of SBP per se,” they suggested.
The J-shaped association observed remained after multiple adjustments, including presence of known cardiovascular comorbidities, which suggested a possible “real effect” of low SBP on severe COVID-19, “at least in treated hypertensive individuals.”
Their analyses also identified that, compared with a “normal” diastolic blood pressure (80-90 mm Hg), having a diastolic blood pressure higher than 90 mm Hg was associated with higher odds of severe COVID-19.
The association between hypertension and COVID-19 was “amplified” if the individuals were treated and their BP remained uncontrolled, the authors pointed out.
There did not appear to be any difference in the risk of severe COVID-19 between individuals taking ACE inhibitors and those taking ARBs or other antihypertensive medications, the authors said.
Better understanding of underlying mechanisms needed
Individuals with hypertension who tested positive for COVID-19 had “over twice” the risk of developing severe COVID-19, compared with nonhypertensive individuals, the authors said.
They highlighted that their findings also suggest that there are “further effects” influencing the severity of COVID-19 beyond a “dichotomous” diagnosis of hypertension.
“Individuals with a higher-than-target systolic blood pressure may be less healthy, less active, suffering more severe hypertension, or have developed drug-resistant hypertension, all suggesting that the effects of hypertension have already had detrimental physiological effects on the cardiovascular system, which in turn may offer some explanation for the higher risk of severe COVID-19 with uncontrolled SBP,” they explained.
“Hypertension is an important risk factor for COVID-19,” reiterated the authors, who emphasized that a better understanding of the underlying mechanisms driving this increased risk is warranted in case of “more severe strains or other viruses” in the future.
The authors have declared no competing interests.
A version of this article first appeared on Medscape UK.
U.K. researchers have established that hypertension is associated with a 22% greater risk of severe COVID-19, with the odds of severe COVID-19 unaffected by medication type.
Hypertension “appears to be one of the commonest comorbidities in COVID-19 patients”, explained the authors of a new study, published in PLOS ONE. The authors highlighted that previous research had shown that hypertension was more prevalent in severe and fatal cases compared with all cases of COVID-19.
They pointed out, however, that whether hypertensive individuals have a higher risk of severe COVID-19, compared with nonhypertensives, and whether the absolute level of systolic blood pressure or the type of antihypertensive medication is related to this risk, remained “unclear.”
To try to answer these questions, the research team, led by University of Cambridge researchers, analyzed data from 16,134 individuals who tested positive for COVID-19 (mean age 65.3 years, 47% male, 90% white), 40% were diagnosed with essential hypertension at the analysis baseline – 22% of whom had developed severe COVID-19.
Systolic blood pressure (SBP) was categorized by 10–mm Hg ranges, starting from < 120 mm Hg up to 180+ mm Hg, with the reference category defined as 120-129 mm Hg, based on data from the SPRINT study, which demonstrated that intensive SBP lowering to below 120 mm Hg, as compared with the traditional threshold of 140 mm Hg, was beneficial. Diastolic blood pressure was categorized by 10–mm Hg ranges, starting from < 60 mm Hg up to 100+ mm Hg with 80-90 mm Hg being the reference category.
In their analyses the researchers adjusted for age, sex, body mass index, ethnicity, smoking status, diabetes status, socioeconomic status, and inflammation (C-reactive protein [CRP]), as these were proposed as potential confounders. To assess the direct effect of hypertension on COVID-19, they also adjusted for intermediate variables, including cardiovascular comorbidities and stroke, on the causal pathway between hypertension and severe COVID-19.
Majority of effect of hypertension on severe COVID-19 was direct
The unadjusted odds ratio of the association between hypertension and severe COVID-19 was 2.33 (95% confidence interval, 2.16-2.51), the authors emphasized. They found that, after adjusting for all confounding variables, hypertension was associated with 22% higher odds of severe COVID-19 (OR, 1.22; 95% CI, 1.12-1.33), compared with normotension.
Individuals with severe COVID-19 were marginally older, more likely to be male, and more deprived, the authors said. “They were also more likely to be hypertensive, compared with individuals without severe COVID-19, and a greater proportion of individuals with severe COVID-19 had cardiovascular comorbidities.”
The majority of the effect of hypertension on development of severe COVID-19 was “direct,” they said. However, a modest proportion of the effect was mediated via cardiovascular comorbidities such as peripheral vascular disease, MI, coronary heart disease, arrhythmias, and stroke. Of note, those with a history of stroke had a 47% higher risk of severe COVID-19 and those with a history of other cardiovascular comorbidities had a 30% higher risk of severe COVID-19, the authors commented.
J-shaped relationship
Of the total of 6,517 (40%) individuals who had a diagnosis of essential hypertension at baseline, 67% were treated (41% with monotherapy, 59% with combination therapy), and 33% were untreated.
There were similar numbers of severe COVID-19 in each medication group: ACE inhibitors, 34%; angiotensin receptor blockers (ARBs), 36%; and “other” medications 34%.
In hypertensive individuals receiving antihypertensive medications, there was a “J-shaped relationship” between the level of blood pressure and risk of severe COVID-19 when using a systolic blood pressure level of 120-129 mm Hg as a reference – 150-159 mm Hg versus 120-129 mm Hg (OR 1.91; 95% CI, 1.44-2.53), > 180+ mm Hg versus 120-129 mm Hg (OR 1.93; 95% CI, 1.06-3.51).
The authors commented that there was no evidence of a higher risk of severe COVID-19 until systolic blood pressure “exceeded 150 mm Hg.”
They said it was an interesting finding that “very well-controlled” systolic blood pressure < 120 mm Hg was associated with a 40% (OR, 1.40; 95% CI, 1.11-1.78) greater odds of severe COVID-19. “This may be due to reverse causality, where low systolic blood pressure levels may indicate poorer health, such that the occurrence of severe COVID-19 may be related to underlying disease rather than the level of SBP per se,” they suggested.
The J-shaped association observed remained after multiple adjustments, including presence of known cardiovascular comorbidities, which suggested a possible “real effect” of low SBP on severe COVID-19, “at least in treated hypertensive individuals.”
Their analyses also identified that, compared with a “normal” diastolic blood pressure (80-90 mm Hg), having a diastolic blood pressure higher than 90 mm Hg was associated with higher odds of severe COVID-19.
The association between hypertension and COVID-19 was “amplified” if the individuals were treated and their BP remained uncontrolled, the authors pointed out.
There did not appear to be any difference in the risk of severe COVID-19 between individuals taking ACE inhibitors and those taking ARBs or other antihypertensive medications, the authors said.
Better understanding of underlying mechanisms needed
Individuals with hypertension who tested positive for COVID-19 had “over twice” the risk of developing severe COVID-19, compared with nonhypertensive individuals, the authors said.
They highlighted that their findings also suggest that there are “further effects” influencing the severity of COVID-19 beyond a “dichotomous” diagnosis of hypertension.
“Individuals with a higher-than-target systolic blood pressure may be less healthy, less active, suffering more severe hypertension, or have developed drug-resistant hypertension, all suggesting that the effects of hypertension have already had detrimental physiological effects on the cardiovascular system, which in turn may offer some explanation for the higher risk of severe COVID-19 with uncontrolled SBP,” they explained.
“Hypertension is an important risk factor for COVID-19,” reiterated the authors, who emphasized that a better understanding of the underlying mechanisms driving this increased risk is warranted in case of “more severe strains or other viruses” in the future.
The authors have declared no competing interests.
A version of this article first appeared on Medscape UK.
U.K. researchers have established that hypertension is associated with a 22% greater risk of severe COVID-19, with the odds of severe COVID-19 unaffected by medication type.
Hypertension “appears to be one of the commonest comorbidities in COVID-19 patients”, explained the authors of a new study, published in PLOS ONE. The authors highlighted that previous research had shown that hypertension was more prevalent in severe and fatal cases compared with all cases of COVID-19.
They pointed out, however, that whether hypertensive individuals have a higher risk of severe COVID-19, compared with nonhypertensives, and whether the absolute level of systolic blood pressure or the type of antihypertensive medication is related to this risk, remained “unclear.”
To try to answer these questions, the research team, led by University of Cambridge researchers, analyzed data from 16,134 individuals who tested positive for COVID-19 (mean age 65.3 years, 47% male, 90% white), 40% were diagnosed with essential hypertension at the analysis baseline – 22% of whom had developed severe COVID-19.
Systolic blood pressure (SBP) was categorized by 10–mm Hg ranges, starting from < 120 mm Hg up to 180+ mm Hg, with the reference category defined as 120-129 mm Hg, based on data from the SPRINT study, which demonstrated that intensive SBP lowering to below 120 mm Hg, as compared with the traditional threshold of 140 mm Hg, was beneficial. Diastolic blood pressure was categorized by 10–mm Hg ranges, starting from < 60 mm Hg up to 100+ mm Hg with 80-90 mm Hg being the reference category.
In their analyses the researchers adjusted for age, sex, body mass index, ethnicity, smoking status, diabetes status, socioeconomic status, and inflammation (C-reactive protein [CRP]), as these were proposed as potential confounders. To assess the direct effect of hypertension on COVID-19, they also adjusted for intermediate variables, including cardiovascular comorbidities and stroke, on the causal pathway between hypertension and severe COVID-19.
Majority of effect of hypertension on severe COVID-19 was direct
The unadjusted odds ratio of the association between hypertension and severe COVID-19 was 2.33 (95% confidence interval, 2.16-2.51), the authors emphasized. They found that, after adjusting for all confounding variables, hypertension was associated with 22% higher odds of severe COVID-19 (OR, 1.22; 95% CI, 1.12-1.33), compared with normotension.
Individuals with severe COVID-19 were marginally older, more likely to be male, and more deprived, the authors said. “They were also more likely to be hypertensive, compared with individuals without severe COVID-19, and a greater proportion of individuals with severe COVID-19 had cardiovascular comorbidities.”
The majority of the effect of hypertension on development of severe COVID-19 was “direct,” they said. However, a modest proportion of the effect was mediated via cardiovascular comorbidities such as peripheral vascular disease, MI, coronary heart disease, arrhythmias, and stroke. Of note, those with a history of stroke had a 47% higher risk of severe COVID-19 and those with a history of other cardiovascular comorbidities had a 30% higher risk of severe COVID-19, the authors commented.
J-shaped relationship
Of the total of 6,517 (40%) individuals who had a diagnosis of essential hypertension at baseline, 67% were treated (41% with monotherapy, 59% with combination therapy), and 33% were untreated.
There were similar numbers of severe COVID-19 in each medication group: ACE inhibitors, 34%; angiotensin receptor blockers (ARBs), 36%; and “other” medications 34%.
In hypertensive individuals receiving antihypertensive medications, there was a “J-shaped relationship” between the level of blood pressure and risk of severe COVID-19 when using a systolic blood pressure level of 120-129 mm Hg as a reference – 150-159 mm Hg versus 120-129 mm Hg (OR 1.91; 95% CI, 1.44-2.53), > 180+ mm Hg versus 120-129 mm Hg (OR 1.93; 95% CI, 1.06-3.51).
The authors commented that there was no evidence of a higher risk of severe COVID-19 until systolic blood pressure “exceeded 150 mm Hg.”
They said it was an interesting finding that “very well-controlled” systolic blood pressure < 120 mm Hg was associated with a 40% (OR, 1.40; 95% CI, 1.11-1.78) greater odds of severe COVID-19. “This may be due to reverse causality, where low systolic blood pressure levels may indicate poorer health, such that the occurrence of severe COVID-19 may be related to underlying disease rather than the level of SBP per se,” they suggested.
The J-shaped association observed remained after multiple adjustments, including presence of known cardiovascular comorbidities, which suggested a possible “real effect” of low SBP on severe COVID-19, “at least in treated hypertensive individuals.”
Their analyses also identified that, compared with a “normal” diastolic blood pressure (80-90 mm Hg), having a diastolic blood pressure higher than 90 mm Hg was associated with higher odds of severe COVID-19.
The association between hypertension and COVID-19 was “amplified” if the individuals were treated and their BP remained uncontrolled, the authors pointed out.
There did not appear to be any difference in the risk of severe COVID-19 between individuals taking ACE inhibitors and those taking ARBs or other antihypertensive medications, the authors said.
Better understanding of underlying mechanisms needed
Individuals with hypertension who tested positive for COVID-19 had “over twice” the risk of developing severe COVID-19, compared with nonhypertensive individuals, the authors said.
They highlighted that their findings also suggest that there are “further effects” influencing the severity of COVID-19 beyond a “dichotomous” diagnosis of hypertension.
“Individuals with a higher-than-target systolic blood pressure may be less healthy, less active, suffering more severe hypertension, or have developed drug-resistant hypertension, all suggesting that the effects of hypertension have already had detrimental physiological effects on the cardiovascular system, which in turn may offer some explanation for the higher risk of severe COVID-19 with uncontrolled SBP,” they explained.
“Hypertension is an important risk factor for COVID-19,” reiterated the authors, who emphasized that a better understanding of the underlying mechanisms driving this increased risk is warranted in case of “more severe strains or other viruses” in the future.
The authors have declared no competing interests.
A version of this article first appeared on Medscape UK.
FROM PLOS ONE