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COVID-19 booster vaccinations mitigate transmission and reduce the morbidity and mortality associated with infection. However, the optimal date for booster administration remains uncertain. Geographic variation in infection rates throughout the year make it challenging to intuit the best yearly booster administration date to effectively prevent infection, and also challenging to provide best guidance in how to alter booster administration in response to a breakthrough infection. Therefore, we leverage longitudinal antibody and reinfection probabilities with spatiotemporal projections of COVID-19 incidence to develop a geographically-informed approach to optimizing the timing of booster vaccination. Additionally, we assess the delay in booster vaccination that is warranted following breakthrough infections whenever they occur during the year, enabling an approach that acknowledges and respects diverse immune statuses, thereby addressing a substantial barrier to uptake. Our results provide guidance for individual decision-making and healthcare provider recommendations, as well as optimal public health policies. Significance Statement COVID-19 booster vaccinations are pivotal in reducing disease transmission. However, optimal schedules that would most successfully mitigate adverse health outcomes have not been rigorously determined. Spatial and temporal surges of infections, including breakthrough infections, challenge the implementation of effective boosting strategies. We leverage antibody data and incidence projections to develop a geographically-informed schedule for yearly booster administration and quantify appropriate delays in booster vaccination post-breakthrough infection, thereby accounting for immune status and enhancing vaccination inclusivity. Our findings offer crucial information for individual decision making, healthcare provider guidance, and policy aimed at optimizing the impact of booster vaccination on public health. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement National Science Foundation of the United States of America RAPID 2031204 (JPT and AD), NSF Expeditions CCF 1918784 (JPT and APG), and support from the University of North Carolina, Charlotte to AD. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes 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, Mathematica notebooks, imputed monthly proportions, and code underlying this study are publicly available on Zenodo: DOI:10.5281/zenodo.11209811.

Nature Communications - Using SARS-CoV-2 viral genome data, Goliaei et al analyze the changes in SARS-CoV-2 lineage importation into Germany after implementation of different nonpharmaceutical...

Postacute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (PASC) can affect many organ systems. However, temporal changes during the coronavirus disease 2019 (Cov...

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DMZ – WISSENSCHAFT ¦ S. Koller Die Studie „Driving Under the Cognitive Influence of COVID-19: Exploring the Impact of Acute SARS-CoV-2 Infection on Road Safety“ untersucht die potenziellen Auswirkungen einer akuten COVID-19-Infektion auf die Fahrsicherheit und beleuchtet die neurologischen Veränderungen, die durch die Infektion verursacht werden könnten. Die Forschung analysierte Verkehrsunfälle in den Jahren 2020 bis 2022 und setzte diese in Bezug zu den COVID-19-Fallzahlen, Long-COVID-Raten und der Durchimpfung der Bevölkerung. Die Ergebnisse zeigen eine signifikante Verbindung zwischen akuten COVID-19-Infektionen und einer erhöhten Zahl von Verkehrsunfällen. Die Studienautoren fanden heraus, dass das Risiko eines Unfalls bei COVID-19-Patienten um etwa 25 % (OR 1,23–1,26) höher war als bei nicht infizierten Personen. Diese Risikozunahme wurde mit der Unfallwahrscheinlichkeit von Personen verglichen, die unter dem Einfluss von Alkohol stehen oder an epileptischen Anfällen leiden. Obwohl diese Vergleiche auf ersten Studien beruhen, sind sie ein Hinweis darauf, dass COVID-19 auch kurzfristige neurologische Auswirkungen haben könnte, die das Unfallrisiko erhöhen. Interessanterweise zeigte sich, dass eine COVID-19-Impfung das erhöhte Unfallrisiko bei akuter Infektion nicht senkte, obwohl dies in früheren Annahmen vermutet wurde. Dies könnte darauf hindeuten, dass die Impfung zwar schwere Krankheitsverläufe verhindert, aber die neurologischen Auswirkungen während einer akuten Infektion nicht vollständig ausschließt. Weitere Forschung ist notwendig, um diese Diskrepanz besser zu verstehen. Die Studie betont die neurologischen Folgen einer akuten SARS-CoV-2-Infektion, die das Fahren stark beeinträchtigen können, selbst wenn keine langanhaltenden Long-COVID-Symptome auftreten. Die Forscher empfehlen daher, die neurologischen Beeinträchtigungen bei post-COVID-Patienten genauer zu untersuchen. Insbesondere wird medizinischen Fachkräften geraten, Patienten, die nach einer Infektion an neurologischen Einschränkungen leiden, bezüglich ihrer Fahrtauglichkeit zu beraten. In schwerwiegenden Fällen könnte eine Meldung an Behörden in Betracht gezogen werden, wenn die Fahrsicherheit erheblich beeinträchtigt ist. Diese Studie verdeutlicht, dass die Auswirkungen der Pandemie auf die Verkehrssicherheit noch nicht vollständig verstanden sind. Es besteht ein dringender Handlungsbedarf, um die öffentliche Sicherheit im Straßenverkehr auch in Zeiten von COVID-19 sicherzustellen. Zur Studie

The SARS-CoV-2 coronavirus emerged in 2019, causing a COVID-19 pandemic that resulted in 7 million deaths out of 770 million reported cases over the next four years. The global health emergency...

Peripheral blood mononuclear cells (PBMC) mitochondrial respiration was measured ex vivo from participants without a history of COVID (n = 19), with a…

DMZ – WISSENSCHAFT ¦ Sarah Koller ¦ Eine Studie hat die Atmungsfunktion von peripheren mononukleären Zellen (PBMC) bei drei Gruppen untersucht: Personen ohne COVID-Vorgeschichte (n = 19), Personen, die sich vollständig von COVID erholt haben (n = 20), und Personen mit PASC (Post-Akute Sequelae der SARS-CoV-2-Infektion) (n = 20). Bei Personen mit PASC war die mittlere mitochondriale Basalatmung, ATP-gebundene Atmung, maximale Atmung, Reserveatmungskapazität, ATP-gebundene Atmung und nicht-mitochondriale Atmung am höchsten (p ≤ 0,04). Eine Erhöhung bestimmter Atmungsfunktionen erhöhte die vorhergesagten Chancen von PASC um 1 % bis 6 %. Die Studie deutet darauf hin, dass eine mitochondriale Dysfunktion in PBMCs zur Ätiologie von PASC beitragen könnte. Eine Teilmenge von Personen, die sich von einer akuten SARS-CoV-2-Infektion erholen, entwickelt eine Reihe von Symptomen, die über viele Monate anhalten, bekannt als Post-Akute Sequelae von SARS-CoV-2 (PASC) oder Long-COVID. Mehr als die Hälfte der COVID-19-Überlebenden hat sechs Monate nach der Genesung PASC, und 29 % der Personen erleben PASC mehr als 12 Monate nach der Infektion. In den Vereinigten Staaten haben schätzungsweise 18,5 Millionen Erwachsene PASC, während weltweit mehr als 65 Millionen Personen darunter leiden. Insgesamt tritt PASC bei mindestens 10 % der SARS-CoV-2-Infektionen auf. Begrenzte Daten zur Mortalität aus dem Nationalen Vitalstatistiksystem schätzen, dass mehr als 3.500 Amerikaner an PASC-bezogenen Erkrankungen gestorben sind. Die genauen Ursachen von PASC sind jedoch nicht gut verstanden, aber mehrere Risikofaktoren wurden identifiziert. Diese Studie war eine prospektive, beobachtende Kohortenstudie. Die Teilnehmer wurden von April 2020 bis November 2020 im University Hospitals Cleveland Medical Center in Cleveland, OH, USA, eingeschrieben. Alle Protokolle wurden vom Institutional Review Board am University Hospitals Cleveland Medical Center, Cleveland, Ohio, genehmigt. Die Teilnehmer wurden durch nasopharyngealen Abstrich mittels Echtzeit-Polymerase-Kettenreaktion (qRT-PCR) auf SARS-CoV-2-Infektion bestätigt. Die COVID-19-Teilnehmer wurden als Teil eines lokalen COVID-19-Biorepositoriums eingeschrieben, das jeden willigen Patienten mit dokumentierter früherer SARS-CoV-2-Infektion unabhängig von aktuellen Symptomen oder Schweregrad der initialen Episode prospektiv einschrieb. PASC wurde anhand der Definition des Centers for Disease Control and Prevention (CDC) definiert. COVID + Teilnehmer galten als PASC, wenn die Genesung nach der 4-wöchigen akuten Phase nicht erfolgte und mindestens zwei anhaltende Symptome vorlagen, die auf PASC zurückzuführen sind und seit der initialen akuten COVID-Erkrankung bis zur aktuellen Studieneinschreibung bestehen. In dieser Studie wurden die mitochondriale Atmung bei Teilnehmern ohne COVID-Vorgeschichte, Teilnehmern, die sich von COVID erholt haben, und bei Teilnehmern mit PASC bewertet. Die mittlere Basalatmung, ATP-gebundene Atmung, maximale Atmung, Reserveatmungskapazität, Protonenleckage und nicht-mitochondriale Atmung bei PASC PBMC sind am höchsten. Im Vergleich zu COVID + no PASC war der Anteil der Atmung, der an die ATP-gebundene Atmung gebunden war, bei PASC signifikant höher. Diese Ergebnisse legen nahe, dass die energetischen Anforderungen von PASC-PBMCs größer sind als die von COVID + no PASC und COVID - PBMCs. Die mitochondriale Dysfunktion wurde bei akuten SARS-CoV-2-Infektionen bereits umfassend untersucht. Diese Dysfunktion ist teilweise auf die umfangreiche virale Ausrichtung der Mitochondrien und mitochondrialen Proteine zurückzuführen. Weiterhin unterstützen diese Ergebnisse die Theorie eines Anstiegs der relativen Anzahl oder Aktivität von zirkulierenden Monozyten bei PASC, da Monozyten die größte Anzahl an Mitochondrien haben und ihren Stoffwechsel in Reaktion auf Stimulation umprogrammieren, um inflammatorische Antworten zu unterstützen. Insgesamt liefern die vorläufigen Ergebnisse neue Erkenntnisse über die zelluläre Bioenergetik bei PASC und legen nahe, dass eine vertiefte Untersuchung der mitochondrialen Dysfunktion bei PASC von entscheidender Bedeutung ist. Weitere Forschungen sind unerlässlich, um die zugrunde liegenden Mechanismen von PASC besser zu verstehen und individualisierte Therapien zu entwickeln. Die vorliegende Studie zeigt eine veränderte mitochondriale Atmung in PBMCs von Personen mit PASC im Vergleich zu Personen ohne PASC oder ohne COVID-Vorgeschichte. Diese Ergebnisse legen nahe, dass mitochondriale Dysfunktion eine Rolle bei der Pathogenese von PASC spielen könnte. Zur Studie

Britische Forscher untersuchten verschiedene Biomarker einer neuroglialen Schädigung sowie Entzündungsmediatoren und Autoantikörper bei Neuro-COVID.

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(mega-thread) — Emmanuel (@ejustin46)

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