Covid19-Sources

"Schweizer Ärzte rätseln: Diabetes (Typ 1, der Typ der nix mit Lockdowns, Bewegungsmangel & Ernährung zu tun hat) bei Schweizer Kindern (2-10 Jahre) explodiert" (~ ca 30%+)Wen hatten Sie zuerst unter den CovidBus geworfen? Aber erfunden haben sie's nicht https://t.co/6XfrEMd8kJ— Dr.med.Hank Schiffers, MD, MBA, Lean Sensei (@leanhealth) April 22, 2024

In 2023 gab es wohl ein Rekordhoch von Arbeitsunfähigkeiten. Seht Ihr den Elefanten im Raum?

At the beginning of 2022, the word ‘endemic’ became a buzzword, especially in the UK and the USA, and a kernel for the formation of novel social representations of the COVID-19 pandemic. The word normally refers to a disease which is continuously present, whose incidence is relatively stable and is maintained at a baseline level in any given locality. Over time, ‘endemic’ migrated from scientific discourse into political discourse, where it was mainly used to argue that the pandemic was over and people now had to learn to ‘live with’ the virus. In this article, we examine the emerging meanings, images and social representations of the term ‘endemic’ in English language news between 1 March 2020 and 18 January 2022. We observe a change over time, from the representation of ‘endemic’ as something dangerous and to be avoided to something desirable and to be aspired to. This shift was facilitated by anchoring COVID-19, especially its variant Omicron, to ‘just like the flu’ and by objectifying it through metaphors depicting a path or journey to normality. However, the new language of hope and aspiration did not go entirely unchallenged. Our analysis suggests that two competing polemic social representations emerged: one of endemicity as hope and aspiration and the other focusing on misguided optimism. We discuss these findings in the context of emerging polarisations in beliefs about the pandemic, politics and disease management. Data sharing not applicable as no datasets generated and/or analysed for this study.

Scientific Reports - SARS-CoV-2 booster vaccine dose significantly extends humoral immune response half-life beyond the primary series

Corona Virus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has presented unprecedented challenges to t...

Nature Immunology - Openshaw and colleagues find myeloid inflammation and complement activation signatures in patients with long COVID who were previously hospitalized.

A new study on long COVID reveals unique immune patterns related to symptoms, advocating for personalized treatment approaches and further research into the condition's biological mechanisms. People with long COVID have distinct patterns of inflammation detectable in the blood, which could potent

Monoclonal antibodies (mAbs) targeting the SARS-CoV-2 receptor-binding domain (RBD) showed high efficacy in the prevention and treatment of COVID-19. However, the rapid evolution of SARS-CoV-2 has rendered all clinically authorized mAbs ineffective and continues to stymie the development of next-generation mAbs. Consequently, the ability to identify broadly neutralizing antibodies (bnAbs) that neutralize both current and future variants is critical for successful antibody therapeutic development, especially for newly emerged viruses when no knowledge about immune evasive variants is available. Here, we have developed a strategy to specifically select for potent bnAbs with activity against both existing and prospective SARS-CoV-2 variants based on accurate viral evolution prediction informed by deep mutational scanning (DMS). By adopting this methodology, we increased the probability of identifying XBB.1.5-effective SARS-CoV-2 bnAbs from ~1% to 40% if we were at the early stage of the pandemic, as revealed by a retrospective analysis of 1,000 SARS-CoV-2 wildtype (WT)-elicited mAbs. From this collection, we identified a bnAb, designated BD55-1205, that exhibited exceptional activity against historical, contemporary, and predicted future variants. Structural analyses revealed extensive polar interactions between BD55-1205 and XBB.1.5 receptor-binding motif (RBM), especially with backbone atoms, explaining its unusually broad reactivity. Importantly, mRNA-based delivery of BD55-1205 IgG to human FcRn-expressing transgenic mice resulted in high serum neutralizing titers against selected XBB and BA.2.86 subvariants. Together, the ability to identify bnAbs via accurate viral evolution prediction, coupled with the speed and flexibility of mRNA delivery technology, provides a generalized framework for the rapid development of next-generation antibody-based countermeasures against SARS-CoV-2 and potentially other highly variable pathogens with pandemic potential. ### Competing Interest Statement Y.C. is listed as an inventor of provisional patent applications of SARS-CoV-2 RBD-specific antibodies involved in the study, including BD55-1205. The patent of BD55-1205 is licensed to Moderna. Y.C. is a co-founder of Singlomics Biopharmaceuticals. A.Z.W., J.H., D.M.B., D.L., T.S., L.M., T.K., K.W., C.H., S.P., and L.M.W. are full-time employees and holders of equity in Moderna Therapeutics. Other authors declare no competing interests.

This paper presents quasiexperimental evidence of Covid-19 transmission through casual contact between customers in retail stores. For a large sample of individuals in Denmark, we match card payment data, indicating exactly where and when each individual made purchases, with Covid-19 test data, indicating when each individual was tested and whether the test was positive. The resulting dataset identifies more than 100,000 instances where an infected individual made a purchase in a store and, in each instance, allows us to track the infection dynamics of other individuals who made purchases in the same store around the same time. We estimate transmissions by comparing the infection rate of exposed customers, who made a purchase within 5 min of an infected individual, and nonexposed customers, who made a purchase in the same store 16 to 30 min before. We find that exposure to an infected individual in a store increases the infection rate by around 0.12 percentage points (P 0.001) between day 3 and day 7 after exposure. The estimates imply that transmissions in stores contributed around 0.04 to the reproduction number for the average infected individual and significantly more in the period where Omicron was the dominant variant.

Over the first half of the 20th century the world saw growing rates of heart disease mortality. From the 1920s to the 1960s more and more people were dying from heart attacks. It was described as an epidemic of heart disease. But in the mid-1960s heart disease mortality suddenly plateaued.

Marsters et al. studied the frequency and outcomes of neurological disease associated with COVID-19 in over 355,000 people, and determined that individuals

SARS-CoV-2 infection is clinically heterogeneous, ranging from asymptomatic to deadly. A few patients withCOVID-19 appear to recover from acute viral infectionbut nevertheless progress in their disease and eventuallydie, despite persistent negativity at molecular tests for SARS-CoV-2 RNA. Here, we performed post-mortemanalyses in 27 consecutive patients who had apparently recovered from COVID-19 but had progressivelyworsened in their clinical conditions despite repeated viral negativity in nasopharyngeal swabs orbronchioalveolar lavage for 11–300 consecutive days (average: 105.5 days). Three of these patients remainedPCR-negative for over 9 months. Post-mortem analysis revealed evidence of diffuse or focal interstitialpneumonia in 23/27 (81%) patients, accompanied by extensivefibrotic substitution in 13 cases (47%). Despiteapparent virological remission, lung pathology was similar to that observed in acute COVID-19 individuals,including micro- and macro-vascular thrombosis (67% of cases), vasculitis (24%), squamous metaplasia ofthe respiratory epithelium (30%), frequent cytological abnormalities and syncytia (67%), and the presence ofdysmorphic features in the bronchial cartilage (44%). Consistent with molecular test negativity, SARS-CoV-2antigens were not detected in the respiratory epithelium. In contrast, antibodies against both spike andnucleocapsid revealed the frequent (70%) infection of bronchial cartilage chondrocytes and para-bronchialgland epithelial cells. In a few patients (19%), we also detected positivity in vascular pericytes and endothelialcells. Quantitative RT-PCR amplification in tissue lysates confirmed the presence of viral RNA. Together, thesefindings indicate that SARS-CoV-2 infection can persist significantly longer than suggested by standardPCR-negative tests, with specific infection of specific cell types in the lung. Whether these persistently infectedcells also play a pathogenic role in long COVID remains to be addressed.

People who are immune-deficient/disordered (IDP) are underrepresented in COVID-19 studies. Specifically, there is limited research on post–SARS-CoV-2 infection outcomes, including viral persistence and long-term sequelae in these populations. Objectives This review aimed to examine the published literature on the occurrence of persistent SARS-CoV-2 positivity, relapse, reinfections, variant coinfection, and post-acute sequelae of COVID-19 in IDP. Although the available literature largely centred on those with secondary immunodeficiencies, studies on people with inborn errors of immunity are also included. Sources PubMed was searched using medical subject headings terms to identify relevant articles from the last 4 years. Articles on primary and secondary immunodeficiencies were chosen, and a special emphasis was placed on including articles that studied people with inborn errors of immunity. The absence of extensive cohort studies including these individuals has limited most articles in this review to case reports, whereas the articles focusing on secondary immunodeficiencies include larger cohort, case-control, and cross-sectional studies. Articles focusing solely on HIV/AIDS were excluded.

Strong sex differences in the frequencies and manifestations of Long COVID (LC) have been reported with females significantly more likely than males to present with LC after acute SARS-CoV-2 infection[1][1]–[7][2]. However, whether immunological traits underlying LC differ between sexes, and whether such differences explain the differential manifestations of LC symptomology is currently unknown. Here, we performed sex-based multi-dimensional immune-endocrine profiling of 165 individuals[8][3] with and without LC in an exploratory, cross-sectional study to identify key immunological traits underlying biological sex differences in LC. We found that female and male participants with LC experienced different sets of symptoms, and distinct patterns of organ system involvement, with female participants suffering from a higher symptom burden. Machine learning approaches identified differential sets of immune features that characterized LC in females and males. Males with LC had decreased frequencies of monocyte and DC populations, elevated NK cells, and plasma cytokines including IL-8 and TGF-β-family members. Females with LC had increased frequencies of exhausted T cells, cytokine-secreting T cells, higher antibody reactivity to latent herpes viruses including EBV, HSV-2, and CMV, and lower testosterone levels than their control female counterparts. Testosterone levels were significantly associated with lower symptom burden in LC participants over sex designation. These findings suggest distinct immunological processes of LC in females and males and illuminate the crucial role of immune-endocrine dysregulation in sex-specific pathology. ### Competing Interest Statement In the past three years, H.K. received expenses and/or personal fees from UnitedHealth, Element Science, Eyedentifeye, and F-Prime. He is a co-founder of Refactor Health and HugoHealth, and is associated with contracts, through Yale New Haven Hospital, from the Centers for Medicare & Medicaid Services and through Yale University from the Food and Drug Administration, Johnson & Johnson, Google, and Pfizer. N.K. is a scientific founder at Thyron, served as a consultant to Boehringer Ingelheim, Pliant, Astra Zeneca, RohBar, Veracyte, Galapagos, Fibrogen, and Thyron over the last 3 years, reports equity in Pliant and Thyron, and acknowledges grants from Veracyte, Boehringer Ingelheim, BMS. A. I. co-founded RIGImmune, Xanadu Bio and PanV, consults for Paratus Sciences, InvisiShield Technologies, and is a member of the Board of Directors of Roche Holding Ltd and Genentech. ### Funding Statement This work was supported by the Else Kroner Fresenius Prize for Medical Research 2023, grants from the National Institute of Allergy and Infectious Diseases (R01AI157488 to A.I.), FDA Office of Womens Health Research Centers of Excellence in Regulatory Science and Innovation (CERSI) (to A.I.), RTW Foundation (D.P.), the Howard Hughes Medical Institute Collaborative COVID-19 Initiative (to A.I. and R.M.), and the Howard Hughes Medical Institute (to A.I. and R.M.). Steve and Alexandra Cohen Foundation (D.P. and J.W.), Nash Family Foundation (D.P. and J.W.) and Polybio Research Foundation (D.P. and J.W.) ### 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: This study was approved by the Mount Sinai Program for the Protection of Human Subjects (IRB #20-01758) and Yale Institutional Review Board (IRB #2000029451 for MY-LC). Informed consent was obtained from all enrolled participants. 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 of the raw fcs files for the flow cytometry analysis are available at the FlowRepository platform () under Repository ID: FR-FCM-Z6KL. [1]: #ref-1 [2]: #ref-7 [3]: #ref-8

DMZ – GESUNDHEIT / WISSEN ¦ David Aebischer ¦ In den letzten Monaten ist uns eine besorgniserregende Tendenz aufgefallen: Die Verharmlosung des Coronavirus, die nicht nur unter Experten und Politikern, sondern auch in den Medien zunehmend Raum zu finden scheint. Während die Welt weiterhin mit den Auswirkungen der Pandemie zu kämpfen hat, scheint die Ernsthaftigkeit des Virus in einigen Kreisen in den Hintergrund zu rücken. Diese Entwicklung wirft wichtige Fragen auf und fordert zum Nachdenken über die Auswirkungen und Herausforderungen auf, denen wir in diesem neuen Stadium der Pandemie gegenüberstehen. Um sicherzustellen, dass unsere Berichterstattung sachlich, unaufgeregt und auf Fakten basiert, haben wir erneut Expertenrat eingeholt und uns mit unseren dringenden Fragen an den renommierten Prof. Antoine Flahault, MD, PhD, Epidemiologe und Direktor des Instituts für globale Gesundheit in Genf, gewandt. DMZ: In welchem Maße stellen Sie eine Tendenz zur Verharmlosung des Coronavirus innerhalb der Expertengemeinschaft fest? Prof. Antoine Flahault: Die durch COVID-19 verursachte übermäßige Sterblichkeit wird bisher auf weltweit über 27 Millionen Todesfälle geschätzt (https://ourworldindata.org/grapher/excess-deaths-cumulative-economist-single-entity), und sowohl die Expertengemeinschaft als auch die Bevölkerung und die politischen Führer haben offenbar nicht aus einer solchen Tragödie gelernt. Die Welt wollte die Seite wenden, sobald die WHO im letzten Frühling das Ende der „gesundheitliche Notlage internationaler Tragweite“ erklärt hat. Natürlich haben wir den Gesundheitsnotstand verlassen, der zu Beginn der Pandemie strenge Einschränkungen unserer Bewegungen und unserer öffentlichen Freiheiten auferlegte. Dennoch bleibt COVID-19 für einige nach wie vor eine gefürchtete und tödliche Krankheit, und das SARS-CoV-2 breitet sich nach wie vor aktiv auf dem Planeten aus, in allen Ländern, wobei es anhaltende Formen verursacht, die als Langzeit-COVID bezeichnet werden und die wir schlecht behandeln können. Es mutiert auch weiterhin in raschem Tempo und erzeugt neue Varianten, die zu neuen Wellen von Neuinfektionen, Krankenhauseinweisungen und Todesfällen zu jeder Jahreszeit führen.

Brazil pic.twitter.com/rSb9HfqN6f— Maresurfer {...} (@maresurfer) April 17, 2024

Nature Communications - Many emerging SARS-CoV-2 variants partially escape the humoral immune response. Here, Liu et al. characterize 28 antibodies from BA.4/5 breakthrough infections and find...

The question of whether SARS-CoV-2 is mainly transmitted by droplets or aerosols has been highly controversial. We sought to explain this controversy through a historical analysis of transmission res...

1/🧵Your brain “on COVID”🧠  Let’s integrate 20 studies on #LongCOVID neuropathology My 24 y/o patient explained: “I don’t have a future because I can’t think anymore.” Let’s talk:Autopsy StudiesViral persistenceBrain Size & DisabilityRecovery & HopeH/T pic 👁️ tw 13 pic.twitter.com/WnMIhO9Bdt— WesElyMD (@WesElyMD) February 6, 2023

Yang et al. characterize the interaction between G3BP1 and SARS-CoV-2 N protein at the single-residue level. They show that a point mutation (N-F17A) selectively disrupts G3BP1-N interaction and reduces viral replication and pathology in vivo, demonstrating that this interaction promotes infection by limiting sequestration of viral gRNA into stress granules.

Sigal, Pardi, and colleagues show that in mice, CD8+ T-cells do not participate in the pathology of primary SARS-CoV-2 infection and that mRNA-LNP vaccine-induced CD8+ T-cells are dispensable when protective antibodies are present but essential for survival in their absence.

Researchers are trying to understand the profound effects of COVID-19 on the brain, looking at how it disrupts the blood-brain barrier, how it affects brain volume, and showing that even a mild case of COVID can lead to the equivalent of seven years of brain aging.

Die umstrittene Behauptung von Sucharit Bhakdi, Thailand wolle den Vertrag mit Pfizer über den Impfstoff Covid-19 kündigen, weil die thailändische Prin...

SARS-CoV-2 cell tropism and infection cycle are defined at the cellular resolution by infection of healthy human lung tissue and single-cell profiling. Int

New Severity Scale for ME/CFSI wrote this new severity scale for ME/CFS about 2 years ago.  I really wanted to express how severe the illness can actually get which is not at all reflected in our current mild-moderate-severe-v.severe scale.  And I wanted to make it more… pic.twitter.com/C0YPoXsrll— Whitney Dafoe (@DafoeWhitney) April 9, 2024

Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients experience multiple complex symptoms, potentially linked to imbalances in brain neurochemicals. This study aims to measure brain neurochemical levels in long COVID and ME/CFS patients as well as healthy controls to investigate associations with severity measures.

Nature Immunology - Openshaw and colleagues find myeloid inflammation and complement activation signatures in patients with long COVID who were previously hospitalized.