Covid19-Sources

This cohort study examines outpatient health care use across 6 categories of care between US veterans with or without COVID-19 infection.

This randomized clinical trial assesses whether ensitrelvir reduces time to resolution of 5 common COVID-19 symptoms among patients with mild to moderate disease in less than 72 hours of disease onset.

Treatment shortened symptoms by a day and also reduced viral loads.

And this might help us treat the symptoms.

Autoantibodies have been shown to be implied in COVID-19 but the emerging autoantibody repertoire remains largely unexplored. We investigated the new-onset autoantibody repertoire in 525 healthcare workers and hospitalized COVID-19 patients in five time points over 16 months using proteome-wide and targeted protein and peptide arrays. Our results show that prevalent new-onset autoantibodies against a wide range of antigens emerged following SARS-CoV-2 infection in relation to pre-infectious baseline samples and remained elevated for at least 12 months. We demonstrated associations between distinct new-onset autoantibodies and neuropsychiatric symptoms post-COVID-19. Using epitope mapping, we determined the main epitopes of selected new-onset autoantibodies, validated them in independent cohorts of neuro-COVID and pre-pandemic healthy controls, and identified molecular mimicry between main epitopes and the conserved fusion peptide of the SARS-CoV-2 Spike glycoprotein. Our work describes the complexity and dynamics of the autoantibody repertoire emerging with COVID-19 and supports the need for continued analysis of the new-onset autoantibody repertoire to elucidate the mechanisms of the post-COVID-19 condition. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was funded by a grant from the Swedish Research Council. ### 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 Swedish Ethical Review Authority gave ethical approval for this work under approval numbers: 2020-01653; 2021-04113; 2017-043 with amendments 2019-00169, 2020-01623, 2020-02719, 2020-05730, 2021-01469, and 2020-01883; 2014/148; and 2022-00526-01. 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 All data produced in the present study are available upon reasonable request to the authors and approval by the relevant ethical boards. Data cannot be shared freely as it contains sensitive personal data covered by the GDPR.

Myalgic Encephalomyelitis/ Chronic Fatigue syndrome (ME/CFS) is a complex, debilitating, long-term illness without a diagnostic biomarker. ME/CFS patients share overlapping symptoms with long COVID patients, an observation which has strengthened the infectious origin hypothesis of ME/CFS. However, the exact sequence of events leading to disease development is largely unknown for both clinical conditions. Here we show antibody response to herpesvirus dUTPases, particularly to that of Epstein-Barr virus (EBV) and HSV-1, increased circulating fibronectin (FN1) levels in serum and depletion of natural IgM against fibronectin ((n)IgM-FN1) are common factors for both severe ME/CFS and long COVID. We provide evidence for herpesvirus dUTPases-mediated alterations in host cell cytoskeleton, mitochondrial dysfunction and OXPHOS. Our data show altered active immune complexes, immunoglobulin-mediated mitochondrial fragmentation as well as adaptive IgM production in ME/CFS patients. Our findings provide mechanistic insight into both ME/CFS and long COVID development. Finding of increased circulating FN1 and depletion of (n)IgM-FN1 as a biomarker for the severity of both ME/CFS and long COVID has an immediate implication in diagnostics and development of treatment modalities. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement We thank Amar Foundation, USA for a career development grant (BKP), ME Research UK (BKP) and Bundesministerium fuer Bildung und Forschung (BMBF) (grant number 01EJ2204E) (BKP) for supporting this work. This research was also supported by the National Institutes of Health (NIH/NIAID), USA, grant RO1AI084898-06 (MEA and MW) and The infectious Diseases Society of America (IDSA) Foundation, USA, grant (MEA). The COVIDOM study is part of the National Pandemic Cohort Network (NAPKON). NAPKON is funded by COVID-19-related grants from the Network University Medicine (NUM; NAPKON grant number: 01KX2021). Parts of the infrastructure of the Wuerzburg study site was funded by the federal state of Bavaria. The STAAB Cohort study was supported by the German Ministry of Research and Education within the Comprehensive Heart Failure Centre Wuerzburg (BMBF 01EO1004 and 01EO1504). This study was, further, supported by the German Research Foundation (DFG) through the Comprehensive Research Center 1525 'Cardio-immune interfaces' (453989101, project C5) (CM and NB) and the Interdisciplinary Center for Clinical Research - IZKF Wuerzburg (advanced clinician-scientist program; AdvCSP 3) (CM). ### 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: COVIDOM study was approved by the local ethics committees of the university hospitals of Kiel (No. D 537/20), and Wuerzburg (No. 236/20_z) and was registered at clinicaltrials.gov ([NCT04679584][1]) and at the German Registry for Clinical Studies (DRKS, DRKS00023742). ME/CFS study was approved by the Ethics Committee of Charite Universitaetsmedizin Berlin (EA2/067/20; EA2\_066\_22; EA4\_174\_22) and TUM (112/14 (healthy controls) and 529/18 (pediatric ME/CFS), 485/18 adult ME/CFS) in accordance with the 1964 Declaration of Helsinki and its later amendments. The STAAB cohort study protocol and procedures comply with the Declaration of Helsinki and received positive votes from the Ethics Committee of the Medical Faculty as well as from the data protection officer of the University of Wuerzburg (vote #98/13). 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 Complete experimental data together with statistical data are uploaded to Mendeley (doi: 10.17632/4xkft5g9r5.1) and is currently under embargo till 13th June 2024. The data will be freely available to all the readers afterwards. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT04679584&atom=%2Fmedrxiv%2Fearly%2F2023%2F06%2F29%2F2023.06.23.23291827.atom

The spectrum, pathophysiology, and recovery trajectory of persistent post-COVID-19 cognitive deficits are unknown, limiting our ability to develop prevention and treatment strategies. We report the one-year cognitive, serum biomarker, and neuroimaging findings from a prospective, national long...

This analysis presents population prevalence estimates of immunosuppression among US adults using data from the 2021 National Health Interview Survey.

Nature Communications - In this longitudinal, case-controlled, cohort design study, authors show that post-exertional malaise is associated with severe exercise-induced myopathy, local and systemic...

"We're seeing clear changes in the muscles in these patients," Michèle van Vugt, professor of internal medicine at Amsterdam UMC, said in a statement.

The development of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in record time to cope with the ongoing coronavirus d…

Long Covid is a big problem in U.S. kids and teens – yet it is still severely underdiagnosed. Now, researchers are collaborating to publish a comprehensive report on long Covid symptoms, hoping to better the diagnosis quota and treatment.

Newly emerged SARS-CoV-2 variants like JN.1, and more recently, the hypermutated BA.2.87.1, have raised global concern. We recruited two groups of participants who had BA.5/BF.7 breakthrough infection post three doses of inactivated vaccines: one group experienced subsequent XBB reinfection, while the other received the XBB-containing trivalent WSK-V102C vaccine. Our comparative analysis of their serum neutralization activities revealed that the WSK-V102C vaccine induced stronger antibody responses against a wide range of variants, notably including JN.1 and the highly escaped BA.2.87.1. Furthermore, our investigation into specific mutations revealed that fragment deletions in NTD significantly contribute to the immune evasion of the BA.2.87.1 variant. Our findings emphasize the necessity for ongoing vaccine development and adaptation to address the dynamic nature of SARS-CoV-2 variants. ### Competing Interest Statement The authors have declared no competing interest.

In the post-pandemic era, growing apprehension exists regarding the potential sequelae of COVID-19. However, the risks of respiratory diseases followi…

Rates of infection have risen and warning to stay away from work and school if you exhibit symptoms

Aging | doi:10.18632/aging.205297. Franziska Hornung, Nilay Köse-Vogel, Claude Jourdan Le Saux, Antje Häder, Lea Herrmann, Luise Schulz, Lukáš Radosa, Thurid Lauf, Tim Sandhaus, Patrick Samson, Torsten Doenst, Daniel Wittschieber, Gita Mall, Bettina Löffler, Stefanie Deinhardt-Emmer

Post-COVID-19 Syndrome (PCS) is characterized by symptoms including fatigue, reduced physical performance, dyspnea, cognitive impairment, and psychological distress. The mechanisms underlying the onset and severity of PCS point to mitochondrial dysfunction as significant contributor. This study examined fat oxidation as a function of mitochondrial capacity during exercise. Methods Single-center prospective cohort study during inpatient rehabilitation. Cardiopulmonary exercise testing and assessment of fatigue using questionnaires were performed at admission and discharge. Detailed spirometric breath-by-breath data were used to calculate substrate oxidation rates. Results Patients (N = 187; 38 % women; 49.7 ± 11.4 years) were referred to rehabilitation 253.4 ± 130.6 days after infection. Lead symptoms included fatigue/exercise intolerance (79.9 %), shortness of breath (77.0 %), and cognitive dysfunction (55.1 %). Fat oxidation capacity was disturbed in PCS patients overall (AUC: 11.3 [10.7–11.9]) compared to healthy controls (p 0.0001), with hospitalization during acute infection predicting the level of disturbance (p 0.0001). Low exercise capacity and high fatigue scores resulted in reduced fat oxidation (both p 0.0001). In particular, younger males were affected by significantly reduced fat oxidation capacity (sex: p = 0.002; age: p 0.001). Metabolic disturbance was significantly improved during exercise-based rehabilitation (AUC: 14.9 [14.4–15.4]; p 0.0001), even for the group of younger impaired males (+44.2 %; p 0.0001). Carbohydrate oxidation was not impaired. Conclusions PCS-specific restrictions in fat oxidation may indicate persistent mitochondrial dysfunction. Clinical assessment of PCS patients should include detailed breath-by-breath analysis during exercise to identify metabolic alterations especially in the group of younger males identified in this report. Exercise-based rehabilitation results in improved exercise capacity and fat oxidation and thus likely mitochondrial function. Clinical Trials: NCT06468722.

Alice in Wonderland Syndrome (AIWS) is a disorienting neurological condition that affects human perception to the senses of vision, hearing, touch, se…

Scientific Reports - In vitro analysis suggests that SARS-CoV-2 infection differentially modulates cancer-like phenotypes and cytokine expression in colorectal and prostate cancer cells

Post-acute COVID-19 syndrome (PACS) has been linked to microvascular endothelial dysfunction as a potential underlying pathomechanism and can manifest even following a mild course of the initial infection. Prevalence of microvascular endothelial dysfunction and circulating natriuretic peptides in such PACS patients remains unknown. Methods and results This prospective, cross-sectional cohort study enrolled 92 patients (82% females, median age 48 years) with PACS. Reactive hyperemia index (RHI) was evaluated with peripheral arterial tonometry where 1.67 was defined as microvascular endothelial dysfunction, 1.67-2.0 impaired- and 2 normal endothelial function, on average 31 months after the acute infection. N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were collected at two different time points within over 1-year span. In total, 41% of PACS subjects had microvascular endothelial dysfunction and 20% had impaired RHI. No major differences in clinical characteristics, routine chemistry laboratory testing or symptom burden were observed across the groups. Only subjects with microvascular endothelial dysfunction and impaired endothelial function had a significant increase in NT-proBNP levels over time and those with larger increase in NT-proBNP had significantly lower RHI. There was a significant correlation between relative or absolute increase in NT-proBNP and RHI, which remained significant in a multivariable adjusted linear regression. Conclusions Peripheral microvascular endothelial dysfunction was prevalent in a symptomatic PACS population long after recovery from a mild acute infection. Increases in NT-proBNP levels were associated with microvascular endothelial dysfunction, suggesting a link between and providing a foundation for future studies on post viral microvascular endothelial dysfunction in PACS.

Nosocomial infections are costly and airborne transmission is increasingly recognised as important for spread. Air Cleaning Units (ACUs) may reduce transmission but little research has focused on their effectiveness on open wards. Aim Assess whether ACUs reduce nosocomial SARS-CoV-2, or other, infections on older adult inpatient wards. Methods Quasi-experimental before-after study on two intervention-control ward pairs in a UK teaching hospital. Infections were identified using routinely collected electronic health records data during one year of ACU implementation and the preceding year (“core study period”). Extended analyses included 6 months additional data from one ward pair following ACU removal. Hazard ratios (HR) were estimated through Cox regression controlling for age, sex, ward and background infection risk. Time the ACUs were switched on was also recorded for intervention ward 2. Findings ACUs were initially feasible but compliance reduced towards the end of the study (average operation in first vs second half of ACU time on intervention ward 2: 77% vs 53%). 8171 admissions 48hrs (6112 patients, median age 85yrs) were included. Overall, incidence of ward-acquired SARS-CoV-2 was 3.8%. ACU implementation was associated with a non-significant trend of lower hazard for SARS-CoV-2 infection (HR core study period 0.90, 95% CI 0.53, 1.52; extended study period 0.78, 95% CI 0.53, 1.14). Only 1.5% of admissions resulted in other notable ward-acquired infections. Conclusion ACUs may reduce SARS-CoV-2 infection to a clinically-meaningfully degree. Larger studies could reduce uncertainty, perhaps using a cross-over design, and factors influencing acceptability to staff and patients should be further explored.

Flu in the summer and RSV year-round: More than two years into the pandemic, familiar viruses are acting in unfamiliar ways.

Respiratory virus/bacteria infections like Rhino/Enterovirus, Adenovirus, Mycoplasma pneumoniae or Pertussis are skyrocketing. 🧵1/ — Joanna Teglund🕊️🍉Human life is sacred😷 (@JoannaTeglund)

CD4+ and CD8+ T cells protect against SARS-CoV-2 viral persistence within the upper respiratory tract.

Lately, I’ve been seeing a lot of posts on social media that ask “why do people who were masking suddenly stop after having covid?” This is definitely “a thing” – one that I’ve seen occur among man…

There is a lot we could to prevent constant reinfections, but no public motivation to do so

npj Viruses - SARS-CoV-2 infection results in a unique lung proteome long after virus resolution in the hamster

The spike design used in the vaccines has a couple of tweaks to make it more stable, and those changes prevent it the vaccine-based spike protein from causing cell fusion! 13/ — Nick #RespiratorsFilterPathogens😷 Anderegg (@NickAnderegg)