Covid19-Sources

Background As SARS-CoV-2 has transitioned from a pandemic to endemic disease, the majority of new infections have been among previously infected individuals. To manage the risks and benefits of ongoing COVID-19 policies, it is important to understand whether prior infection modifies the severity of subsequent infections. Methods We used data from first and second COVID-19 episodes in the National COVID Cohort Collaborative (N3C), a collection of health systems who provide de-identified electronic health records for research purposes. Our analysis was a sequential series of nested trial emulations. In the first of two analytic stages, we created a month-specific model of the probability of prior infection for each individual. In the second stage, we used an ordinal logistic regression with inverse probability weights calculated in the first stage to simulate a series of monthly trials comparing severity between the cohorts of first and second infections. In addition to cohort-wide effect estimates, we also conducted analyses among race/ethnicity, sex, and age subgroups. Results From an initial cohort of 7,446,481 combined first and second infections, we identified a cohort of 2,227,484 infections, among which 7.6% were second infections. Ninety-four percent of patients with two recorded infections experienced mild disease for both. The overall odds ratio (OR) for more severe disease with prior infection was 1.06 (95% confidence interval [CI]: 1.03 – 1.10). Monthly point estimates of the OR ranged from 0.56 (95% CI: 0.37 – 0.84) in October 2020 to 1.64 (95% CI: 1.33 – 2.00) in February 2023. In most subgroups, the effect of prior infection was significant. In 8 out of 10 subgroups, the maximum monthly OR occurred after the minimum monthly OR, suggesting that protection has waned throughout the pandemic. Conclusion Overall, prior infection was associated with a significant slightly elevated risk of severe disease. This effect varied month to month. As the pandemic proceeded, the effect of prior infection tended to evolve from generally protective during the pre-Omicron era to unprotective during the Omicron era. This points to the need for continued strategies to avert and minimize the harms of COVID-19, rather than relying upon immunity acquired through previous infection. Question Does prior infection with SARS-CoV-2 affect the severity of subsequent COVID-19 episodes? Findings We observed a mild protective effect of prior infection during the early and mid-stages of the pandemic that waned after the rise of the Omicron variants, ultimately resulting in loss of protection or a tendency toward more severe second infections. Meaning Prior infection alone is likely not enough to avert the worst public health harms of endemic SARS-CoV-2. Interventions to avoid infection and reduce the severity of COVID-19 will still be important in the post-pandemic era. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This project was sponsored by an award from the National COVID Cohort Collaborative's Public Health Answers to Speed Tractable Results (PHASTR) program and the National Center for Advancing Translational Sciences (Award #NCATS-P00438-E-2). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The study design was exempted from human subjects research review by the American Academy of Family Medicine institutional review board. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Data are available online through the National COVID Cohort Collaborative () with signed data use agreement and project approval.

In the Research Article “The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2,” the frequency of simulated topologies matching phylogenetic structures arising from a single introduction was incorrectly reported because of an error in the code, which has been corrected. Correspondingly, the Bayes factors in favor of multiple introductions of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the human population relative to a single introduction were overestimated. The text now represents the corrected Bayes factors and topology frequency (Fig. 2C), which still favors the multiple introduction scenario. Bayes factor significance cutoffs from Kass and Raftery (1995) are now used throughout the text, including Table 1, where the probability of inferred ancestral haplotypes is reported. These cutoffs highlight the disagreement between the rooting inferred when using only human viruses (lineage B rooting) by comparison with incorporating the bat viruses through the recombinant common ancestor (lineage A rooting). This analysis independently supports the conclusion that lineages A and B were most likely the result of at least two cross-species transmissions of SARS-CoV-2.

Objective Vaccination reduces the risk of acute COVID-19 in children, but it is less clear whether it protects against long COVID. We estimated vaccine effectiveness (VE) against long COVID in children aged 5-17 years. Methods This retrospective cohort study used data from 17 health systems in the RECOVER PCORnet electronic health record (EHR) Program for visits between vaccine availability, and October 29, 2022. Conditional logistic regression was used to estimate VE against long COVID with matching on age group (5-11, 12-17) and time period and adjustment for sex, ethnicity, health system, comorbidity burden, and pre-exposure health care utilization. We examined both probable (symptom-based) and diagnosed long COVID in the year following vaccination. Results The vaccination rate was 56% in the cohort of 1,037,936 children. The incidence of probable long COVID was 4.5% among patients with COVID-19, while diagnosed long COVID was 0.7%. Adjusted vaccine effectiveness within 12 months was 35.4% (95 CI 24.5 – 44.5) against probable long COVID and 41.7% (15.0 – 60.0) against diagnosed long COVID. VE was higher for adolescents 50.3% [36.3 – 61.0]) than children aged 5-11 (23.8% [4.9 – 39.0]). VE was higher at 6 months (61.4% [51.0 – 69.6]) but decreased to 10.6% (–26.8 – 37.0%) at 18-months. Discussion This large retrospective study shows a moderate protective effect of SARS-CoV-2 vaccination against long COVID. The effect is stronger in adolescents, who have higher risk of long COVID, and wanes over time. Understanding VE mechanism against long COVID requires more study, including EHR sources and prospective data. Article Summary Vaccination against COVID-19 has a protective effect against long COVID in children and adolescents. The effect wanes over time but remains significant at 12 months. What’s Known on This Subject Vaccines reduce the risk and severity of COVID-19 in children. There is evidence for reduced long COVID risk in adults who are vaccinated, but little information about similar effects for children and adolescents, who have distinct forms of long COVID. What This Study Adds Using electronic health records from US health systems, we examined large cohorts of vaccinated and unvaccinated patients

In this nationwide register-based cohort study of 2 430 694 Danish adults aged ≥50 years, we found no support for a persisting increased susceptibility to clini

Over 1,000 cases of pediatric hepatitis of unknown etiology have been reported worldwide since the first case was reported in the UK. To date, the etiology of pediatric hepatitis remains unknown and controversial. Adenovirus was first suspected to be the cause as it was present in the blood samples of the majority of cases. Partial cases have also been tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. However, it is still unclear how these viruses contribute to pediatric hepatitis. In the case of a pediatric patient with SARS-CoV-2 infection, the liver biopsy showed acute submassive hepatocyte necrosis, accompanied by a significant increase in T cell infiltration [2]. Furthermore, CD8 T-cell dominant hepatitis induced by coronavirus disease 2019 (COVID-19) vaccination has also been recently reported [3]. Although it is known that T cell receptors (TCRs) can discriminate between self- and non-self-antigens, it is now well-accepted that TCRs exhibit cross-reactivity toward similar and even distinct antigen peptides [4]. Thus, we hypothesized that following SARS-CoV-2 infection or vaccination, T cells carrying TCRs that recognize self-antigens undergo clonal expansion, which could eventually result in the onset of autoimmune-like hepatitis

The SARS-CoV-2 genome encodes a multitude of accessory proteins. Using comparative genomic approaches, an additional accessory protein, ORF3c, has been predicted to be encoded within the ORF3a sgmRNA. Expression of ORF3c during infection has been confirmed independently by ribosome profiling. Despite ORF3c also being present in the 2002–2003 SARS-CoV, its function has remained unexplored. Here we show that ORF3c localises to mitochondria, where it inhibits innate immunity by restricting IFN-β production, but not NF-κB activation or JAK-STAT signalling downstream of type I IFN stimulation.

PDF | Purpose The complexity of long COVID and its diverse symptom profile contributes to unprecedented challenges for patients, clinicians, and... | Find, read and cite all the research you need on ResearchGate

This report describes how young infants of people who received a COVID-19 vaccine while pregnant were less likely to be hospitalized or experience serious complications from COVID-19.

You never forget your first time with SARS-CoV-2.

Abstract. Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (C

COVID-19 can have different presentations; from asymptomatic to multiorgan involvement. This case report is of an elderly gentleman, with known comorbidities of chronic obstructive airway diseas...

Interactive tool uses environmental data to calculate survivability of the virus in the air.

npj Vaccines - Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients

Nature - A molnupiravir-associated mutational signature in global SARS-CoV-2 genomes

Study finds evidence virus can survive treatment with molnupiravir, leading to mutated versions that sometimes spread

Nature Immunology - Wherry and colleagues define the kinetics of vaccine-primed recall immune responses during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) breakthrough infection,...

It is not clear why some individuals develop postacute sequelae of COVID-19 (PASC) while others do not. Here, Herman et al. used systems serology to probe antibody features associated with development of PASC in individuals with rheumatic diseases. The authors found that the presence of functional antibodies specific to OC43, an endemic human coronavirus, were enriched in PASC. Although more causal analysis is warranted, these results suggest that immunological imprinting specific to OC43 may be a driver of PASC, particularly in individuals with prior rheumatic disease. —Courtney Malo

Background The COVID-19 pandemic has overwhelmed the respiratory isolation capacity in hospitals; many wards lacking high-frequency air changes have been repurposed for managing patients infected with SARS-CoV-2 requiring either standard or intensive care. Hospital-acquired COVID-19 is a recognised problem amongst both patients and staff, with growing evidence for the relevance of airborne transmission. This study examined the effect of air filtration and ultra-violet (UV) light sterilisation on detectable airborne SARS-CoV-2 and other microbial bioaerosols. Methods We conducted a crossover study of portable air filtration and sterilisation devices in a repurposed ‘surge’ COVID ward and ‘surge’ ICU. National Institute for Occupational Safety and Health (NIOSH) cyclonic aerosol samplers and PCR assays were used to detect the presence of airborne SARS-CoV-2 and other microbial bioaerosol with and without air/UV filtration. Results Airborne SARS-CoV-2 was detected in the ward on all five days before activation of air/UV filtration, but on none of the five days when the air/UV filter was operational; SARS-CoV-2 was again detected on four out of five days when the filter was off. Airborne SARS-CoV-2 was infrequently detected in the ICU. Filtration significantly reduced the burden of other microbial bioaerosols in both the ward (48 pathogens detected before filtration, two after, p =0.05) and the ICU (45 pathogens detected before filtration, five after p =0.05). Conclusions These data demonstrate the feasibility of removing SARS-CoV-2 from the air of repurposed ‘surge’ wards and suggest that air filtration devices may help reduce the risk of hospital-acquired SARS-CoV-2. Funding Wellcome Trust, MRC, NIHR ### Competing Interest Statement Vilas Navapurkar is the founder, Director, and shareholder of Cambridge Infection Diagnostics Ltd. Andrew Conway-Morris, Paul White, Gordon Dougan and Stephen Baker are members of the Scientific Advisory Board of Cambridge Infection Diagnostics Ltd. Theodore Gouliouris has received a research grant from Shionogi. R Andres Floto has received research grants and/or consultancy payments from GSK, AZ, Chiesi, Shionogi, Insmed, Thirty Technology. Effrossyni Gkrania-Klotsas has received a National Institute of Health Research Greenshoots Award ### Clinical Trial Service evaluation of ability of a device to remove bioaerosol not involving patient data ### Funding Statement This work was supported by a Wellcome senior research fellowship to Stephen Baker (215515/Z/19/Z). Andrew Conway Morris is supported by a Clinician Scientist Fellowship from the Medical Research Council (MR/V006118/1). Mailis Maes and Sally Forrest are funded by the National Institute for Health Research [Cambridge Biomedical Research Centre at the Cambridge University Hospitals NHS Foundation Trust]. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: UK National Institute for Health Research confirmed that ethical approval was not required for this work. All necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable. Yes Data is available on request to the corresponding author.

Patients suffering from this complex chronic health condition face barrier after barrier seeking care, including ignorance, stigma, and discrimination

The likelihood of self-reported long COVID after a first coronavirus (COVID-19) infection compatible with the Omicron BA.1 or BA.2 variants, compared with the Delta variant, using data from the COVID-19 Infection Survey.

Nature Biomedical Engineering - A computationally designed antigen based on the receptor binding domain of the spike protein of sarbecoviruses elicits broad humoral responses against severe acute...

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### Key messages High rates of long COVID or post-acute sequelae of COVID-19 (PASC) continue to be reported in academic journals and subsequently filtered to the public. For instance, the Centers for Disease Control and Prevention (CDC) recently stated ‘nearly one in five American adults who have had COVID-19 still have long Covid’.1 Many scientific publications overestimate PASC prevalence because of overly broad definitions, lack of control groups, inappropriate control groups, and other methodological flaws. This problem is further compounded by inclusion of poorly conducted studies into systematic reviews and meta-analyses that overstate the risk. This is fed to the public by the media and social media, raising undue concern and anxiety. This paper aims to discuss these estimation errors and why epidemiologic research on long COVID has been misleading. For the purposes of this paper, we define long COVID as a syndrome or individual symptoms which are direct sequelae of the virus, SARS-CoV-2, and last at least 12 weeks. Some post-COVID sequelae such as post-ICU syndrome, and post-pneumonia respiratory compromise are common to many upper respiratory viruses. While post-infectious conditions common to other respiratory illnesses may be included in estimates of prevalence of lasting symptoms, we propose future research avoid the umbrella term ‘long COVID’ and …

This study shows that SRS-CoV-2 of different lineages can infect tonsils and adenoids in one quarter of children undergoing tonsillectomy. These findings bring advancement to the area of SARS-CoV-2 pathogenesis, by showing that tonsils may be sites of ...

Scientific Reports - A wild boar cathelicidin peptide derivative inhibits severe acute respiratory syndrome coronavirus-2 and its drifted variants

Emory Vaccine Center researchers say they have identified the Achilles heel of SARS-CoV-2, the virus that causes COVID-19.

Association between messenger RNA (mRNA) COVID-19 vaccines and myocarditis has aroused public concern over vaccine safety.The goal of this study was t…

Objective To investigate the clinical outcomes of myocarditis associated with mRNA vaccines against the SARS-CoV-2 virus compared with other types of myocarditis. Design Population based cohort study. Setting Nationwide register data from four Nordic countries (Denmark, Finland, Norway, and Sweden), from 1 January 2018 to the latest date of follow-up in 2022. Participants The Nordic myocarditis cohort; 7292 individuals aged ≥12 years who had an incident diagnosis of myocarditis as a main or secondary diagnosis, in a population of 23 million individuals in Denmark, Finland, Norway, and Sweden. Main outcome measures Heart failure, or death from any cause within 90 days of admission to hospital for new onset myocarditis, and hospital readmission within 90 days of discharge to hospital for new onset myocarditis. Clinical outcomes of myocarditis associated with SARS-CoV-2 mRNA vaccination, covid-19 disease, and conventional myocarditis were compared. Results In 2018-22, 7292 patients were admitted to hospital with new onset myocarditis, with 530 (7.3%) categorised as having myocarditis associated with SARS-CoV-2 mRNA vaccination, 109 (1.5%) with myocarditis associated with covid-19 disease, and 6653 (91.2%) with conventional myocarditis. At the 90 day follow-up, 62, nine, and 988 patients had been readmitted to hospital in each group (vaccination, covid-19, and conventional myocarditis groups, respectively), corresponding to a relative risk of readmission of 0.79 (95% confidence interval 0.62 to 1.00) and 0.55 (0.30 to 1.04) for the vaccination type and covid-19 type myocarditis groups, respectively, compared with the conventional myocarditis group. At the 90 day follow-up, 27, 18, and 616 patients had a diagnosis of heart failure or died in the vaccination type, covid-19 type, and conventional myocarditis groups, respectively. The relative risk of heart failure within 90 days was 0.56 (95% confidence interval 0.37 to 0.85) and 1.48 (0.86 to 2.54) for myocarditis associated with vaccination and covid-19 disease, respectively, compared with conventional myocarditis; the relative risk of death was 0.48 (0.21 to 1.09) and 2.35 (1.06 to 5.19), respectively. Among patients aged 12-39 years with no predisposing comorbidities, the relative risk of heart failure or death was markedly higher for myocarditis associated with covid-19 disease than for myocarditis associated with vaccination (relative risk 5.78, 1.84 to 18.20). Conclusions Compared with myocarditis associated with covid-19 disease and conventional myocarditis, myocarditis after vaccination with SARS-CoV-2 mRNA vaccines was associated with better clinical outcomes within 90 days of admission to hospital. Data may be obtained from a third party and are not publicly available. Individual level data underlying the country specific analyses were only available within each Nordic country. The data do not belong to the authors and they are not permitted to share these data, except as presented in this manuscript.

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“Among working people 35 to 44 years old, a stunning 34% more died than expected in the last quarter of 2022, with above-average rates in other working-age groups, too.” h/t @LongCovidFam https://t.co/J01f6rZWW6— Laura Miers (@LauraMiers) August 11, 2023