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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.
Without guidelines, docs make their own long-COVID protocols
Treating the condition requires equal combinations of skill, experience, and intuition, and doctors waiting for guidelines have started cobbling together treatment plans designed to ease the worst symptoms.
Their work is urgent. In the United States alone, as many as 29 million people have long COVID, according to estimates from the American Academy of Physical Medicine and Rehabilitation.
“Patients with long COVID have on average at least 14 different symptoms involving nine or more different organ systems, so a holistic approach to treatment is essential,” said Janna Friedly, MD, executive director of the Post-COVID Rehabilitation and Recovery Clinic at the University of Washington in Seattle.
For acute COVID cases, the National Institutes of Health has treatment guidelines that are taking a lot of the guesswork out of managing patients’ complex mix of symptoms. This has made it easier for primary care providers to manage people with milder cases and for specialists to come up with effective treatment plans for those with severe illness. But no such guidelines exist for long COVID, and this is making it harder for many doctors – particularly in primary care – to determine the best treatment.
While there isn’t a single treatment that is effective for all long-COVID symptoms – and nothing is approved by the Food and Drug Administration specifically for this syndrome – doctors do have tools, Dr. Friedly said.
“We always start with the basics – making sure we help patients get enough restorative sleep, optimizing their nutrition, ensuring proper hydration, reducing stress, breathing exercises, and restorative exercise – because all of these are critically important to helping people’s immune system stay as healthy as possible,” she said. “In addition, we help people manage the anxiety and depression that may be exacerbating their symptoms.”
Fatigue is an obvious target. Widely available screening tools, including assessments that have been used in cancer patients and people with chronic fatigue syndrome, can pinpoint how bad symptoms are in long-COVID patients.
“Fatigue is generally the No. 1 symptom,” said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center in San Antonio. “If a patient has this, then their therapy program has to look very different, because they actually do better with pacing themselves.”
This was the first symptom tackled in a series of long-COVID treatment guidelines issued by the medical society representing many of the providers on the front lines with these patients every day – the American Academy of Physical Medicine and Rehabilitation. These fatigue guidelines stress the importance of rest, energy conservation, and proper hydration.
For patients with only mild fatigue who can still keep up with essential activities like work and school, activity programs may begin with a gradual return to daily routines such as housework or going out with friends. As long as they have no setbacks, patients can also start with light aerobic exercise and make it more intense and frequent over time. As long as they have no setbacks in symptoms, they can ramp up exercise by about 10% every 10 days.
But with severe fatigue, this is too much, too soon. Activity plans are more apt to start with only light stretching and progress to light muscle strengthening before any aerobic exercise enters the picture.
“Traditional exercise programs may be harmful to some patients with long COVID,” said Dr. Verduzco-Gutierrez. “Many cannot tolerate graded exercise [where exertion slowly ramps up], and it actually can make them worse.”
There’s less consensus on other options for treating fatigue, like prescription medications, dietary supplements, and acupuncture. Some doctors have tried prescription drugs like the antiviral and movement disorder medication amantadine, the narcolepsy drug modafinil, and the stimulant methylphenidate, which have been studied for managing fatigue in patients with other conditions like cancer, multiple sclerosis, traumatic brain injuries, and Parkinson’s disease. But there isn’t yet clear evidence from clinical trials about how well these options work for long COVID.
Similarly, interventions to tackle neurological symptoms and cognitive problems borrow a page from treatments used for other conditions like stroke and dementia – but require changes to meet the needs of those with long COVID. Four in five long-COVID patients with neurological and cognitive issues have brain fog, while more than two-thirds have headaches, and more than half have numbness and tingling in their extremities, loss of taste, loss of smell, and muscle pain, one study suggests.
Patients with deficits in areas like memory, attention, executive function, and visual and spatial planning may get speech therapy or occupational therapy, for example – both approaches that are common in people with cognitive decline caused by other medical conditions.
Doctors also promote good sleep practices and treating any mood disorders – both of which can contribute to cognitive problems. But they often have to skip one of the best interventions for improving brain function – exercise – because so many long-COVID patients struggle with fatigue and exertion or have cardiovascular issues that limit their exercise.
The lack of formal guidelines is especially a problem because there aren’t nearly enough specialists to manage the surge of patients who need treatment for issues like fatigue and brain fog. And without guidelines, primary care providers lack a reliable road map to guide referrals that many patients may need.
“Given the complexity of long COVID and the wide range of symptoms and medical issues associated with long COVID, most physicians, regardless of specialty, will need to evaluate and treat long-COVID symptoms,” said Dr. Friedly. “And yet, most do not have the knowledge or experience to effectively manage long-COVID symptoms, so having guidelines that can be updated as more research is conducted is critical.”
One barrier to developing guidelines for long COVID is the lack of research into the biological causes of fatigue and autonomic dysfunction – nervous system damage that can impact critical things like blood pressure, digestion, and body temperature – that affect so many long-COVID patients, said Alba Miranda Azola, MD, codirector of the Post-Acute COVID-19 Team at Johns Hopkins University in Baltimore.
Research is also progressing much more slowly for long COVID than it did for those hospitalized with severe acute infections. The logistics of running rigorous studies to prove which treatments work best for specific symptoms – information needed to create definitive treatment guidelines – are much more complicated for people with long COVID who live at home and may be too exhausted or too preoccupied with their daily lives to take part in research.
The vast number of symptoms, surfacing in different ways for each patient, also make it hard to isolate specific ways to manage specific long-COVID symptoms. Even when two patients have fatigue and brain fog, they may still need different treatments based on the complex mix of other symptoms they have.
“All long-COVID patients are not equal, and it is critical that research focuses on establishing specific descriptions of the disease,” Dr. Azola said.
The National Institutes of Health is working on this through its long-COVID Recover Initiative. It’s unclear how long it will take for this research to yield enough definitive information to inform long-COVID treatment guidelines similar to what the agency produced for acute coronavirus infections, and it didn’t respond to questions about the timeline.
But over the next few months, the National Institutes of Health expects to begin several clinical trials focused on some of the symptoms that doctors are seeing most often in their clinics, like fatigue, brain fog, exercise intolerance, sleep disturbances, and changes in the nervous system’s ability to regulate key functions like heart rate and body temperature.
One trial starting in January will examine whether the COVID-19 drug Paxlovid can help. A recent preprint Department of Veterans Affairs study showed patients treated with Paxlovid were less likely to get long COVID in the first place.
Some professionals aren’t waiting for the agency. The LongCovid Research Consortium links researchers from Harvard and Stanford universities; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai; Cardiff; and Yale who are studying, for instance, whether tiny blood clots contribute to long COVID and whether drugs can reduce or eliminate them.
“Given the widespread and diverse impact the virus has on the human body, it is unlikely that there will be one cure, one treatment,” said Gary H. Gibbons, MD, director of the National Heart, Lung, and Blood Institute at the National Institutes of Health. “This is why there will be multiple clinical trials over the coming months that study a range of symptoms, underlying causes, risk factors, outcomes, and potential strategies for treatment and prevention, in people of all races, ethnicities, genders, and ages.”
A version of this article first appeared on WebMD.com.
Treating the condition requires equal combinations of skill, experience, and intuition, and doctors waiting for guidelines have started cobbling together treatment plans designed to ease the worst symptoms.
Their work is urgent. In the United States alone, as many as 29 million people have long COVID, according to estimates from the American Academy of Physical Medicine and Rehabilitation.
“Patients with long COVID have on average at least 14 different symptoms involving nine or more different organ systems, so a holistic approach to treatment is essential,” said Janna Friedly, MD, executive director of the Post-COVID Rehabilitation and Recovery Clinic at the University of Washington in Seattle.
For acute COVID cases, the National Institutes of Health has treatment guidelines that are taking a lot of the guesswork out of managing patients’ complex mix of symptoms. This has made it easier for primary care providers to manage people with milder cases and for specialists to come up with effective treatment plans for those with severe illness. But no such guidelines exist for long COVID, and this is making it harder for many doctors – particularly in primary care – to determine the best treatment.
While there isn’t a single treatment that is effective for all long-COVID symptoms – and nothing is approved by the Food and Drug Administration specifically for this syndrome – doctors do have tools, Dr. Friedly said.
“We always start with the basics – making sure we help patients get enough restorative sleep, optimizing their nutrition, ensuring proper hydration, reducing stress, breathing exercises, and restorative exercise – because all of these are critically important to helping people’s immune system stay as healthy as possible,” she said. “In addition, we help people manage the anxiety and depression that may be exacerbating their symptoms.”
Fatigue is an obvious target. Widely available screening tools, including assessments that have been used in cancer patients and people with chronic fatigue syndrome, can pinpoint how bad symptoms are in long-COVID patients.
“Fatigue is generally the No. 1 symptom,” said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center in San Antonio. “If a patient has this, then their therapy program has to look very different, because they actually do better with pacing themselves.”
This was the first symptom tackled in a series of long-COVID treatment guidelines issued by the medical society representing many of the providers on the front lines with these patients every day – the American Academy of Physical Medicine and Rehabilitation. These fatigue guidelines stress the importance of rest, energy conservation, and proper hydration.
For patients with only mild fatigue who can still keep up with essential activities like work and school, activity programs may begin with a gradual return to daily routines such as housework or going out with friends. As long as they have no setbacks, patients can also start with light aerobic exercise and make it more intense and frequent over time. As long as they have no setbacks in symptoms, they can ramp up exercise by about 10% every 10 days.
But with severe fatigue, this is too much, too soon. Activity plans are more apt to start with only light stretching and progress to light muscle strengthening before any aerobic exercise enters the picture.
“Traditional exercise programs may be harmful to some patients with long COVID,” said Dr. Verduzco-Gutierrez. “Many cannot tolerate graded exercise [where exertion slowly ramps up], and it actually can make them worse.”
There’s less consensus on other options for treating fatigue, like prescription medications, dietary supplements, and acupuncture. Some doctors have tried prescription drugs like the antiviral and movement disorder medication amantadine, the narcolepsy drug modafinil, and the stimulant methylphenidate, which have been studied for managing fatigue in patients with other conditions like cancer, multiple sclerosis, traumatic brain injuries, and Parkinson’s disease. But there isn’t yet clear evidence from clinical trials about how well these options work for long COVID.
Similarly, interventions to tackle neurological symptoms and cognitive problems borrow a page from treatments used for other conditions like stroke and dementia – but require changes to meet the needs of those with long COVID. Four in five long-COVID patients with neurological and cognitive issues have brain fog, while more than two-thirds have headaches, and more than half have numbness and tingling in their extremities, loss of taste, loss of smell, and muscle pain, one study suggests.
Patients with deficits in areas like memory, attention, executive function, and visual and spatial planning may get speech therapy or occupational therapy, for example – both approaches that are common in people with cognitive decline caused by other medical conditions.
Doctors also promote good sleep practices and treating any mood disorders – both of which can contribute to cognitive problems. But they often have to skip one of the best interventions for improving brain function – exercise – because so many long-COVID patients struggle with fatigue and exertion or have cardiovascular issues that limit their exercise.
The lack of formal guidelines is especially a problem because there aren’t nearly enough specialists to manage the surge of patients who need treatment for issues like fatigue and brain fog. And without guidelines, primary care providers lack a reliable road map to guide referrals that many patients may need.
“Given the complexity of long COVID and the wide range of symptoms and medical issues associated with long COVID, most physicians, regardless of specialty, will need to evaluate and treat long-COVID symptoms,” said Dr. Friedly. “And yet, most do not have the knowledge or experience to effectively manage long-COVID symptoms, so having guidelines that can be updated as more research is conducted is critical.”
One barrier to developing guidelines for long COVID is the lack of research into the biological causes of fatigue and autonomic dysfunction – nervous system damage that can impact critical things like blood pressure, digestion, and body temperature – that affect so many long-COVID patients, said Alba Miranda Azola, MD, codirector of the Post-Acute COVID-19 Team at Johns Hopkins University in Baltimore.
Research is also progressing much more slowly for long COVID than it did for those hospitalized with severe acute infections. The logistics of running rigorous studies to prove which treatments work best for specific symptoms – information needed to create definitive treatment guidelines – are much more complicated for people with long COVID who live at home and may be too exhausted or too preoccupied with their daily lives to take part in research.
The vast number of symptoms, surfacing in different ways for each patient, also make it hard to isolate specific ways to manage specific long-COVID symptoms. Even when two patients have fatigue and brain fog, they may still need different treatments based on the complex mix of other symptoms they have.
“All long-COVID patients are not equal, and it is critical that research focuses on establishing specific descriptions of the disease,” Dr. Azola said.
The National Institutes of Health is working on this through its long-COVID Recover Initiative. It’s unclear how long it will take for this research to yield enough definitive information to inform long-COVID treatment guidelines similar to what the agency produced for acute coronavirus infections, and it didn’t respond to questions about the timeline.
But over the next few months, the National Institutes of Health expects to begin several clinical trials focused on some of the symptoms that doctors are seeing most often in their clinics, like fatigue, brain fog, exercise intolerance, sleep disturbances, and changes in the nervous system’s ability to regulate key functions like heart rate and body temperature.
One trial starting in January will examine whether the COVID-19 drug Paxlovid can help. A recent preprint Department of Veterans Affairs study showed patients treated with Paxlovid were less likely to get long COVID in the first place.
Some professionals aren’t waiting for the agency. The LongCovid Research Consortium links researchers from Harvard and Stanford universities; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai; Cardiff; and Yale who are studying, for instance, whether tiny blood clots contribute to long COVID and whether drugs can reduce or eliminate them.
“Given the widespread and diverse impact the virus has on the human body, it is unlikely that there will be one cure, one treatment,” said Gary H. Gibbons, MD, director of the National Heart, Lung, and Blood Institute at the National Institutes of Health. “This is why there will be multiple clinical trials over the coming months that study a range of symptoms, underlying causes, risk factors, outcomes, and potential strategies for treatment and prevention, in people of all races, ethnicities, genders, and ages.”
A version of this article first appeared on WebMD.com.
Treating the condition requires equal combinations of skill, experience, and intuition, and doctors waiting for guidelines have started cobbling together treatment plans designed to ease the worst symptoms.
Their work is urgent. In the United States alone, as many as 29 million people have long COVID, according to estimates from the American Academy of Physical Medicine and Rehabilitation.
“Patients with long COVID have on average at least 14 different symptoms involving nine or more different organ systems, so a holistic approach to treatment is essential,” said Janna Friedly, MD, executive director of the Post-COVID Rehabilitation and Recovery Clinic at the University of Washington in Seattle.
For acute COVID cases, the National Institutes of Health has treatment guidelines that are taking a lot of the guesswork out of managing patients’ complex mix of symptoms. This has made it easier for primary care providers to manage people with milder cases and for specialists to come up with effective treatment plans for those with severe illness. But no such guidelines exist for long COVID, and this is making it harder for many doctors – particularly in primary care – to determine the best treatment.
While there isn’t a single treatment that is effective for all long-COVID symptoms – and nothing is approved by the Food and Drug Administration specifically for this syndrome – doctors do have tools, Dr. Friedly said.
“We always start with the basics – making sure we help patients get enough restorative sleep, optimizing their nutrition, ensuring proper hydration, reducing stress, breathing exercises, and restorative exercise – because all of these are critically important to helping people’s immune system stay as healthy as possible,” she said. “In addition, we help people manage the anxiety and depression that may be exacerbating their symptoms.”
Fatigue is an obvious target. Widely available screening tools, including assessments that have been used in cancer patients and people with chronic fatigue syndrome, can pinpoint how bad symptoms are in long-COVID patients.
“Fatigue is generally the No. 1 symptom,” said Monica Verduzco-Gutierrez, MD, chair of rehabilitation medicine and director of the COVID-19 Recovery Clinic at the University of Texas Health Science Center in San Antonio. “If a patient has this, then their therapy program has to look very different, because they actually do better with pacing themselves.”
This was the first symptom tackled in a series of long-COVID treatment guidelines issued by the medical society representing many of the providers on the front lines with these patients every day – the American Academy of Physical Medicine and Rehabilitation. These fatigue guidelines stress the importance of rest, energy conservation, and proper hydration.
For patients with only mild fatigue who can still keep up with essential activities like work and school, activity programs may begin with a gradual return to daily routines such as housework or going out with friends. As long as they have no setbacks, patients can also start with light aerobic exercise and make it more intense and frequent over time. As long as they have no setbacks in symptoms, they can ramp up exercise by about 10% every 10 days.
But with severe fatigue, this is too much, too soon. Activity plans are more apt to start with only light stretching and progress to light muscle strengthening before any aerobic exercise enters the picture.
“Traditional exercise programs may be harmful to some patients with long COVID,” said Dr. Verduzco-Gutierrez. “Many cannot tolerate graded exercise [where exertion slowly ramps up], and it actually can make them worse.”
There’s less consensus on other options for treating fatigue, like prescription medications, dietary supplements, and acupuncture. Some doctors have tried prescription drugs like the antiviral and movement disorder medication amantadine, the narcolepsy drug modafinil, and the stimulant methylphenidate, which have been studied for managing fatigue in patients with other conditions like cancer, multiple sclerosis, traumatic brain injuries, and Parkinson’s disease. But there isn’t yet clear evidence from clinical trials about how well these options work for long COVID.
Similarly, interventions to tackle neurological symptoms and cognitive problems borrow a page from treatments used for other conditions like stroke and dementia – but require changes to meet the needs of those with long COVID. Four in five long-COVID patients with neurological and cognitive issues have brain fog, while more than two-thirds have headaches, and more than half have numbness and tingling in their extremities, loss of taste, loss of smell, and muscle pain, one study suggests.
Patients with deficits in areas like memory, attention, executive function, and visual and spatial planning may get speech therapy or occupational therapy, for example – both approaches that are common in people with cognitive decline caused by other medical conditions.
Doctors also promote good sleep practices and treating any mood disorders – both of which can contribute to cognitive problems. But they often have to skip one of the best interventions for improving brain function – exercise – because so many long-COVID patients struggle with fatigue and exertion or have cardiovascular issues that limit their exercise.
The lack of formal guidelines is especially a problem because there aren’t nearly enough specialists to manage the surge of patients who need treatment for issues like fatigue and brain fog. And without guidelines, primary care providers lack a reliable road map to guide referrals that many patients may need.
“Given the complexity of long COVID and the wide range of symptoms and medical issues associated with long COVID, most physicians, regardless of specialty, will need to evaluate and treat long-COVID symptoms,” said Dr. Friedly. “And yet, most do not have the knowledge or experience to effectively manage long-COVID symptoms, so having guidelines that can be updated as more research is conducted is critical.”
One barrier to developing guidelines for long COVID is the lack of research into the biological causes of fatigue and autonomic dysfunction – nervous system damage that can impact critical things like blood pressure, digestion, and body temperature – that affect so many long-COVID patients, said Alba Miranda Azola, MD, codirector of the Post-Acute COVID-19 Team at Johns Hopkins University in Baltimore.
Research is also progressing much more slowly for long COVID than it did for those hospitalized with severe acute infections. The logistics of running rigorous studies to prove which treatments work best for specific symptoms – information needed to create definitive treatment guidelines – are much more complicated for people with long COVID who live at home and may be too exhausted or too preoccupied with their daily lives to take part in research.
The vast number of symptoms, surfacing in different ways for each patient, also make it hard to isolate specific ways to manage specific long-COVID symptoms. Even when two patients have fatigue and brain fog, they may still need different treatments based on the complex mix of other symptoms they have.
“All long-COVID patients are not equal, and it is critical that research focuses on establishing specific descriptions of the disease,” Dr. Azola said.
The National Institutes of Health is working on this through its long-COVID Recover Initiative. It’s unclear how long it will take for this research to yield enough definitive information to inform long-COVID treatment guidelines similar to what the agency produced for acute coronavirus infections, and it didn’t respond to questions about the timeline.
But over the next few months, the National Institutes of Health expects to begin several clinical trials focused on some of the symptoms that doctors are seeing most often in their clinics, like fatigue, brain fog, exercise intolerance, sleep disturbances, and changes in the nervous system’s ability to regulate key functions like heart rate and body temperature.
One trial starting in January will examine whether the COVID-19 drug Paxlovid can help. A recent preprint Department of Veterans Affairs study showed patients treated with Paxlovid were less likely to get long COVID in the first place.
Some professionals aren’t waiting for the agency. The LongCovid Research Consortium links researchers from Harvard and Stanford universities; the University of California, San Francisco; the J. Craig Venter Institute; Johns Hopkins University; the University of Pennsylvania; Mount Sinai; Cardiff; and Yale who are studying, for instance, whether tiny blood clots contribute to long COVID and whether drugs can reduce or eliminate them.
“Given the widespread and diverse impact the virus has on the human body, it is unlikely that there will be one cure, one treatment,” said Gary H. Gibbons, MD, director of the National Heart, Lung, and Blood Institute at the National Institutes of Health. “This is why there will be multiple clinical trials over the coming months that study a range of symptoms, underlying causes, risk factors, outcomes, and potential strategies for treatment and prevention, in people of all races, ethnicities, genders, and ages.”
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
Meet the JCOM Author with Dr. Barkoudah: Neurosurgery Operating Room Efficiency During the COVID-19 Era
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