Covid19-Sources

In the absence of neutralizing antibodies that protect from infection, quantification of S-binding IgG post vaccination may be useful to identify the most vulnerable for fatal COVID-19 among the oldest and frailest. This information is of importance for future strategies to protect vulnerable populations against neutralization resistant variants of concern.

In the absence of neutralizing antibodies that protect from infection, quantification of S-binding IgG post vaccination may be useful to identify the most vulnerable for fatal COVID-19 among the oldest and frailest. This information is of importance for future strategies to protect vulnerable populations against neutralization resistant variants of concern.

U.S. media has extensively covered racial disparities in COVID-19 infections and deaths, which may ironically reduce public concern about COVID-19. In…

Background  Contrary to immunological expectations, decay of adaptive responses against severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) characterizes recovered patients compared with patients who had a severe disease course or died ...

Nature - The human leukocyte antigen allele HLA-B*15:01 is associated with asymptomatic SARS-CoV-2 infection due to pre-existing T cell immunity.

Infections can lead to persistent or long-term symptoms and diseases such as shingles after varicella zoster, cancers after human papillomavirus, or rheumatic fever after streptococcal infections 1,2 . Similarly, infection by SARS-CoV-2 can result in Long COVID, a condition characterized by symptoms of fatigue and pulmonary and cognitive dysfunction 3–5 . The biological mechanisms that contribute to the development of Long COVID remain to be clarified. We leveraged the COVID-19 Host Genetics Initiative6,7 to perform a genome-wide association study for Long COVID including up to 6,450 Long COVID cases and 1,093,995 population controls from 24 studies across 16 countries. We identified the first genome-wide significant association for Long COVID at the FOXP4 locus. FOXP4 has been previously associated with COVID-19 severity6 , lung function 8 , and cancers 9 , suggesting a broader role for lung function in the pathophysiology of Long COVID. While we identify COVID-19 severity as a causal risk factor for Long COVID, the impact of the genetic risk factor located in the FOXP4 locus could not be solely explained by its association to severe COVID-19. Our findings further support the role of pulmonary dysfunction and COVID-19 severity in the development of Long COVID.

Nature - A genome-wide association study of critically ill patients with COVID-19 identifies genetic signals that relate to important host antiviral defence mechanisms and mediators of inflammatory...

Nature Communications - Measuring an individual’s level of exposure to COVID-19 is challenging, and it is therefore unclear whether high exposure may impact immunity. Here, the authors...

4 Laryngoscope, 133:2357-2361, 2023.

Lingering COVID virus in taste buds can affect sense of taste up to 1.5 years after infection.

Wir haben zur Zeit wie jeden Spätsommer hohe Wachstumsrate bei noch relativ niedriger Inzidenz. Sars-Cov-2 will man nicht haben: Man stirbt zwar heute nicht mehr sofort daran, aber es kann sehr una…

Nature Medicine - Longitudinal proteomic profiling of over 1,800 patients revealed two distinct profiles of blood biomarkers measured on admission to hospital for COVID-19, which predict cognitive...

Nature Medicine - Longitudinal proteomic profiling of over 1,800 patients revealed two distinct profiles of blood biomarkers measured on admission to hospital for COVID-19, which predict cognitive...

An increasing number of reports suggest an association between COVID-19 infection and initiation or acceleration of neurodegenerative diseases including Alzheimer's disease (AD) and Creutzfeldt-Jakob disease (CJD). Both these diseases and several other neurodegenerative diseases are caused by conversion of human proteins into a misfolded, aggregated amyloid fibril state. The fibril formation process is self-perpetuating by seeded conversion from preformed fibril seeds. We recently described a plausible mechanism for amyloid fibril formation of SARS-CoV-2 spike protein. Spike-protein formed amyloid fibrils upon cleavage by neutrophil elastase, abundant in the inflammatory response to COVID-19 infection. We here provide evidence of significant Spike-amyloid fibril seeded acceleration of amyloid formation of CJD associated human prion protein (HuPrP) using an in vitro conversion assay. By seeding the HuPrP conversion assay with other in vitro generated disease associated amyloid fibrils we demonstrate that this is not a general effect but a specific feature of spike-amyloid fibrils. We also showed that the amyloid fibril formation of AD associated Aβ1-42 was accelerated by Spike-amyloid fibril seeds. Of seven different 20-amino acid long peptides, Spike532 (532NLVKNKCVNFNFNGLTGTGV551) was most efficient in seeding HuPrP and Spike601 (601GTNTSNQVAVLYQDVNCTEV620) was most effective in seeding Aβ1-42, suggesting substrate dependent selectivity of the cross-seeding activity. Albeit purely in vitro, our data suggest that cross-seeding by Spike-amyloid fibrils can be implicated in the increasing number of reports of CJD, AD, and possibly other neurodegenerative diseases in the wake of COVID-19. ### Competing Interest Statement The authors have declared no competing interest.

Nice paper from Nature asking why T cells so often overlooked (harder to measure) & how they are the key to fighting COVID (of note, we know in HIV how important T cells are because HIV infects T cells so we think of them all the time)https://t.co/22FQv7scRg— Monica Gandhi MD, MPH (@MonicaGandhi9) February 2, 2022

Falschinformationen können sich heutzutage durch das Internet und die sozialen Medien rasend schnell verbreiten. Insbesondere zum Thema Impfen kursieren eine Vielzahl von Falschinformationen und Behauptungen, die wissenschaftlich nicht belegt sind. Falsches Wissen über Impfungen kann zu Verunsicherung und gesundheitlich bedenklichen Entscheidungen führen.

The aim of this study is to present the case report of a 36-year-old woman developing premature ovarian insufficiency (POI) after COVID-19 and review the literature referring to the possible impact...

Importantly, we found that BA.2.86 exhibits lower cell infectivity compared to XBB.1.5 and EG.5, which may affect its transmission. The lower infectivity may be contributed by K356T, V483del, and E554K. Note that here the infectivity is measured through pseudovirus assays. (6/n) pic.twitter.com/WOPXIPLOtT— Yunlong Richard Cao (@yunlong_cao) August 31, 2023

The spike protein receptor-binding domain (RBD) of SARS-CoV-2 is the molecular target for many vaccines and antibody-based prophylactics aimed at bringing COVID-19 under control. Such a narrow molecular focus raises the specter of viral immune evasion as a potential failure mode for these biomedical interventions. With the emergence of new strains of SARS-CoV-2 with altered transmissibility and immune evasion potential, a critical question is this: how easily can the virus escape neutralizing antibodies (nAbs) targeting the spike RBD? To answer this question, we combined an analysis of the RBD structure-function with an evolutionary modeling framework. Our structure-function analysis revealed that epitopes for RBD-targeting nAbs overlap one another substantially and can be evaded by escape mutants with ACE2 affinities comparable to the wild type, that are observed in sequence surveillance data and infect cells in vitro. This suggests that the fitness cost of nAb-evading mutations is low. We then used evolutionary modeling to predict the frequency of immune escape before and after the widespread presence of nAbs due to vaccines, passive immunization or natural immunity. Our modeling suggests that SARS-CoV-2 mutants with one or two mildly deleterious mutations are expected to exist in high numbers due to neutral genetic variation, and consequently resistance to vaccines or other prophylactics that rely on one or two antibodies for protection can develop quickly -and repeatedly- under positive selection. Predicted resistance timelines are comparable to those of the decay kinetics of nAbs raised against vaccinal or natural antigens, raising a second potential mechanism for loss of immunity in the population. Strategies for viral elimination should therefore be diversified across molecular targets and therapeutic modalities.

The omicron variants of the SARS-CoV-2 virus, which have rapidly spread around the world over the past year, latch onto our cells more tightly, invade them more efficiently, and elude many of the antibodies ...

The viral kinetics since symptom onset characterised for symptomatic patients with COVID-19 in our study show that previously vaccinated or younger individuals, or those with a milder infection, shed fewer viruses in a shorter period, implying possible transmission dynamics of SARS-CoV-2 and protective mechanisms of vaccination against infection and severe outcomes.

Nature - Convergent mutations in hot spots of the spike proteins of currently circulating SARS-CoV-2 Omicron variants increase the binding affinity for the host receptor and promote more efficient...

Nature - Rigorous evidence shows that significant contact with a person with SARS-CoV-2 is more likely to lead to transmission than a short encounter.

The KFF provides reliable, accurate, and non-partisan information to help inform health policy in the US. The KFF has just released its 'Health Misinformation Tracking Poll Pilot' examining the public’s media use and trust in sources of health information and measuring the reach of specific false and inaccurate claims surrounding three health-related topics: COVID-19 and

"I was very impressed by all those professionals working hard to make a difference for other people. I recognised myself in so many of the patient experiences described." – Elke Hausmann provides an

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This hyper-mutated variant has shown up in many places now, at a time when wastewater and genomic surveillance is greatly diminished around the world. To date, the BA.2.86 variant has been detected in Israel, Denmark (3 individuals), the UK, the US (2 individuals, one coming back from Japan), and South Africa (2 individuals). It has also been detected in wastewater in 1 region is Switzerland (2% level), along with wastewater detection in Ohio and in Thailand. It’s safe say BA.2.86’s presence is widespread across the world at this point.

Will the new variant be more like Omicron or one of the less remarkable post-Omicron variants—or a total dud?