Covid19-Sources

Most people who get COVID-19 don't suffer damage to the brain. But some do, and even people who initially get just mild COVID symptoms are vulnerable. COVID's potential to damage the brain is anoth...

Scientific Reports - Consistent FFP2-masking as part of reducing viral respiratory infections on medical wards for allogeneic hematopoietic stem cell transplantation

Molecular Neurobiology - “Brain fog,” a persistent cognitive impairment syndrome, stands out as a significant neurological aftermath of coronavirus disease 2019 (COVID-19). Yet, the...

Nature - Audio and visual stimulation at 40 Hz promote cerebrospinal and interstitial fluid flux in mouse brain and result in amyloid clearance via the glymphatic system in a mouse model of...

▶️ COVID-19 infection triggers an inflammatory response and oxidative stress in the brain, leading to cognitive decline. ▶️ Genes involved in mitochondrial function were consistently downregulated across different brain cells — Emmanuel (@ejustin46)

Fatigue and dyspnea are the most commonly reported long-term complaints in individuals previously infected with SARS-CoV-2. This study aimed to comprehensively evaluate diaphragm muscle function in post-COVID-19 patients and investigate whether potential diaphragm dysfunction contributes to physical functioning impairment. A total of 46 patients who qualified for pulmonary rehabilitation were examined. Diaphragm muscle function parameters were evaluated using ultrasonography, while the severity of dyspnea, aerobic capacity, and the amount of energy used by the body during physical activity were assessed using the six-minute walk test, mMRC scale, and Metabolic Equivalent Task (MET), respectively. We identified that 69.5% of patients had diaphragm atrophy and 6.5% had diaphragm paralysis. The percentage of atrophy was not related to age, gender, BMI, oxygen therapy usage during the COVID-19 infection course, and disease severity. Patients who experienced cough, fever, and no loss of smell during the COVID-19 course had significantly greater diaphragm inspiratory thickness values, while patients with cough and no smell disorders had a significantly lower percentage of diaphragm atrophy. Diaphragm functional parameters were strongly associated with selected variables of exercise tolerance, such as distance in the six-minute walk test, oxygen saturation levels, fatigue, and exertion on the Borg scale. In conclusion, diaphragm muscle dysfunction is a serious long-term post-COVID-19 consequence and can be viewed as a major contributing factor to prolonged functional impairments.

Scientists and Economists Alert! Global Emergency  Compounded by the AIDS-like Features of SARS-CoV-2 Infection Over a million people in the US are being infected with severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) every day.  Originally named after the acute respiratory syndrome it can cause as a consequence of blood vessel damage in the lungs, … Continued

Recent studies suggest an increased risk of reinfection with the SARS-CoV-2 Omicron variant compared with previous variants, potentially due to an increased ability to escape immunity specific to older variants, high antigenic divergence of Omicron from earlier virus variants as well as its altered cell entry pathway. The present study sought to investigate epidemiological evidence for differential SARS-CoV-2 reinfection intervals and incidence rates for the Delta versus Omicron variants within Wales. Reinfections in Wales up to February 2022 were defined using genotyping and whole genome sequencing. The median inter-infection intervals for Delta and Omicron were 226 and 192 days, respectively. An incidence rate ratio of 2.17 for reinfection with Omicron compared to Delta was estimated using a conditional Poisson model, which accounted for several factors including sample collection date, age group, area of residence, vaccination and travel status. These findings are consistent with an increased risk of reinfection with the Omicron variant, and highlight the value of monitoring emerging variants that have the potential for causing further waves of cases.

During the summer of 2024, COVID-19 cases surged globally, driven by variants derived from JN.1 subvariants of SARS-CoV-2 that feature new mutations, particularly in the N-terminal domain (NTD) of the spike protein. In this study, we report on the neutralizing antibody (nAb) escape, infectivity, fusion, and stability of these subvariants—LB.1, KP.2.3, KP.3, and KP.3.1.1. Our findings demonstrate that all of these subvariants are highly evasive of nAbs elicited by the bivalent mRNA vaccine, the XBB.1.5 monovalent mumps virus-based vaccine, or from infections during the BA.2.86/JN.1 wave. This reduction in nAb titers is primarily driven by a single serine deletion (DelS31) in the NTD of the spike, leading to a distinct antigenic profile compared to the parental JN.1 and other variants. We also found that the DelS31 mutation decreases pseudovirus infectivity in CaLu-3 cells, which correlates with impaired cell-cell fusion. Additionally, the spike protein of DelS31 variants appears more conformationally stable, as indicated by reduced S1 shedding both with and without stimulation by soluble ACE2, and increased resistance to elevated temperatures. Molecular modeling suggests that the DelS31 mutation induces a conformational change that stabilizes the NTD and strengthens the NTD-Receptor-Binding Domain (RBD) interaction, thus favoring the down conformation of RBD and reducing accessibility to both the ACE2 receptor and certain nAbs. Additionally, the DelS31 mutation introduces an N-linked glycan modification at N30, which shields the underlying NTD region from antibody recognition. Our data highlight the critical role of NTD mutations in the spike protein for nAb evasion, stability, and viral infectivity, and suggest consideration of updating COVID-19 vaccines with antigens containing DelS31. ### Competing Interest Statement The authors have declared no competing interest.

We developed a genome-wide transcriptomic clock for predicting chronological age using whole blood samples from 463 healthy individuals. Our findings reveal profound age acceleration, up to 24.47 years, under perturbed homeostasis in COVID-19 patients, which reverted to baseline upon recovery. This study demonstrates that the whole blood transcriptome can track reversible changes in biological age induced by stressors in real physiological time, suggesting a potential role for anti-aging interventions in disease management. ### Competing Interest Statement There is potential conflict of interest. * BIC : Bayesian Information Criterion COVID-19 : COronaVIrus Disease of 2019 FDR : False Discovery Rate GO : Gene Ontology KEGG : Kyoto Encyclopedia of Genes and Genomes KGP : Korean Genome Project LARS : Least Angle Regression LASSO : Least Absolute Shrinkage and Selection Operator MAE : Mean Absolute Error PCA : Principal Component Analysis RSEM : RNA-Seq by Expectation-Maximization SASPs : Senescence Associated Secretory Phenotypes STAR : Spliced Transcripts Alignment to a Reference TAA : Transcriptomic Age Acceleration VIS : Virus-Induced Senescence.

Post-COVID-19 condition (also known as long COVID)—the term that encapsulates the long-term health effects caused by SARS-CoV-2 infection—is a complex multisystemic chronic disease with profound consequences.1,2 Shortly after long COVID was first reported, the search begun to find pharmaceutical agents to prevent and treat it. Because SARS-CoV-2 itself is the causative agent of long COVID and because viral persistence is postulated to play a major role in the pathogenesis of the condition, antivirals, which block viral replication, were seen as potential candidates for the prevention and treatment of long COVID.

IMPACT on SEMEN/SPERM quality, ERECTILE DYSFUNCTION, FERTILITY ISSUES Mega-thread with more than 20 studies ! — Emmanuel (@ejustin46)

Copenhagen, Denmark: More than three months after suffering from mild COVID infection, men have lower sperm concentrations and fewer sperm that are able to swim, according to new findings presented today (Monday) at the 39th annual meeting of the European Society of Human Reproduction and Embryology (ESHRE) [1].

Both the health and economic burden from Long Covid in NZ are likely to be large. But we can take action now to reduce the impact.

Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines are pivotal in combating coronavirus disease 2019 (COVID-19); however, the declining antibody titers postvaccination pose challenges for sustained protection and herd immunity. Although gut microbiome is reported to affect the early antibody response after vaccination, its impact on the longevity of vaccine-induced antibodies remains unexplored. Methods A prospective cohort study was conducted involving 44 healthy adults who received two doses of either the BNT162b2 or ChAdOx1 vaccine, followed by a BNT162b2 booster at six months. The gut microbiome was serially analyzed using 16S rRNA and shotgun sequencing, while humoral immune response was assessed using a SARS-CoV-2 spike protein immunoassay. Results Faecalibacterium prausnitzii was associated with robust and persistent antibody responses post-BNT162b2 vaccination. In comparison, Escherichia coli was associated with a slower antibody decay following ChAdOx1 vaccination. The booster immune response was correlated with metabolic pathways involving cellular functions and aromatic amino acid synthesis. Conclusions The findings of this study underscored the potential interaction between the gut microbiome and the longevity/boosting effect of antibodies following vaccination against SARS-CoV-2. The identification of specific microbial associations suggests the prospect of microbiome-based strategies for enhancing vaccine efficacy.

A significant proportion of male COVID-19 patients have low testosterone levels, which can persist for months after recovery from the infection. It is uncertain whether gonadotropin-releasing hormone (GnRH) neurons or their functions are affected in individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The research group from France, the United Kingdom, Spain, Germany, Hungary, and Italy examined the hormone profile of male COVID-19 patients at various times after infection. They also used the postmortem brain tissue of patients who died of COVID-19 to investigate possible infection of GnRH neurons and olfactory epithelia with SARS-CoV-2. The results have shown that persistent hypotestosteronemia in COVID-19 or long COVID syndrome could be of hypothalamic origin due to impaired GnRH function, or hypogonadotropic hypogonadism.

Background Since the discovery of COVID-19 in December 2019, the novel virus has spread globally causing significant medical and socio-economic burden. Although the pandemic has been curtailed, the virus and its attendant complication live on. A major global concern is its adverse impact on male fertility. Aim This study was aimed to give an up to date and robust data regarding the effect of COVID-19 on semen variables and male reproductive hormones. Materials and methods Literature search was performed according to the recommendations of PRISMA. Out of the 852 studies collected, only 40 were eligible for inclusion in assessing the effect SARS-CoV-2 exerts on semen quality and androgens. More so, a SWOT analysis was conducted. Results The present study demonstrated that SARS-CoV-2 significantly reduced ejaculate volume, sperm count, concentration, viability, normal morphology, and total and progressive motility. Furthermore, SARS-CoV-2 led to a reduction in circulating testosterone level, but a rise in oestrogen, prolactin, and luteinizing hormone levels. These findings were associated with a decline in testosterone/luteinizing hormone ratio. Conclusions The current study provides compelling evidence that SARS-CoV-2 may lower male fertility by reducing semen quality through a hormone-dependent mechanism; reduction in testosterone level and increase in oestrogen and prolactin levels.

- Rheumatoid arthritis - Multiple sclerosis - Type 1 diabetes - Celiac disease - ME/CFS - Lupus A new EBV study in multiple sclerosis (MS) reveals an important clue that might explain this… — Brain Inflammation Collaborative (@BrainInflCollab)

— Jan Hartmann (@pelagicbird)

Long-COVID is a broadly defined condition and there are no effective therapies. Cardiovascular manifestations of long-COVID include high heart rate, postural tachycardia, and palpitations. Previous studies have suggested that mast cell activation (MCA) ...

— T. Ryan Gregory (@TRyanGregory)

So far, there has been no discernible increase in suicides among young Germans. Ongoing suicide monitoring is recommended.

Fibrin "binds to the SARS-CoV-2 spike protein," forming clots that "drive systemic thromboinflammation and neuropathology," and it happens "independently of active infection." Simplified breakdown of the paper below! 1/many — Nick #RespiratorsFilterPathogens😷 Anderegg (@NickAnderegg)

Nature - Fibrin drives inflammation and neuropathology in SARS-CoV-2 infection, and fibrin-targeting immunotherapy may represent a therapeutic intervention for patients with long COVID.

The ability of governments to implement climate policies is the “most important” factor in feasibility of limiting global warming to 1.5C.

— Vipin M. Vashishtha (@vipintukur)

Communications Medicine - Yechezkel et al. compare the safety profiles of the BNT162b2 COVID-19 booster and the seasonal influenza vaccine using data from wearables, reported reactions, and...

Employment has increased at a higher rate among the disabled population than the broader population since the onset of COVID-19. Which types of disabilities are associated with the recent increase?