Covid19-Sources

BACKGROUND: COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post–COVID-19 are not known. METHODS: Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR+)-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based International Classification of Diseases version-10 (ICD-10) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score—matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components. RESULTS: The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94–2.25]; P<0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51–4.24]; P<0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08–1.37]; P<0.005). A significant genetic interaction was observed between the ABO locus and hospitalization for COVID-19 (Pinteraction=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29–2.09]; P=4.8×10−5) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66–1.39]; P=0.82). CONCLUSIONS: Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post–acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events. Graphical Abstract

Subtle cognitive dysfunction and mental fatigue are frequent after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, characterizing the so-called long COVID-19 syndrome. This study aimed to correlate cognitive, ...

(mega-thread🧵) Chaos theory in the understanding of the COVID-19 pandemic

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The rapid spread of COVID-19 underscores the need for new treatments. Here we report that cannabidiol (CBD), a compound produced by the cannabis plant, inhibits SARS-CoV-2 infection. CBD and its metabolite, 7-OH-CBD, but not congeneric cannabinoids, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after cellular infection, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription. CBD induces interferon expression and up-regulates its antiviral signaling pathway. A cohort of human patients previously taking CBD had significantly lower SARS-CoV-2 infection incidence of up to an order of magnitude relative to matched pairs or the general population. This study highlights CBD, and its active metabolite, 7-OH-CBD, as potential preventative agents and therapeutic treatments for SARS-CoV-2 at early stages of infection. ### Competing Interest Statement Five of the authors (MRR, GR, LCN, DY and JMM) filed a provisional patent entitled Method of use of Cannabidiol as an antiviral agent. Receipt of the provisional patient was acknowledged by the USPTO on November 30, 2020. S.A.O. is a cofounder and consultant at OptiKira., L.L.C. (Cleveland, OH).

Coronavirus disease-19 (COVID-19) is a highly contagious illness caused by the SARS-CoV-2 virus. The clinical presentation of COVID-19 is variable, often including symptoms such as fever, cough, headache, fatigue, and an altered sense of smell and taste. Recently, post-acute “long” COVID-19 has emerged as a concern, with symptoms persisting beyond the acute infection. Vaccinations remain one of the most effective preventative methods against severe COVID-19 outcomes and the development of long-term COVID-19. However, individuals with underlying health conditions may not mount an adequate protective response to COVID-19 vaccines, increasing the likelihood of severe symptoms, hospitalization, and the development of long-term COVID-19 in high-risk populations. This review explores the potential therapeutic role of cannabinoids in limiting the susceptibility and severity of infection, both pre- and post-SARS-CoV-19 infection. Early in the SARS-CoV-19 infection, cannabinoids have been shown to prevent viral entry, mitigate oxidative stress, and alleviate the associated cytokine storm. Post-SARS-CoV-2 infection, cannabinoids have shown promise in treating symptoms associated with post-acute long COVID-19, including depression, anxiety, post-traumatic stress injury, insomnia, pain, and decreased appetite. While current research primarily focuses on potential treatments for the acute phase of COVID-19, there is a gap in research addressing therapeutics for the early and post-infectious phases. This review highlights the potential for future research to bridge this gap by investigating cannabinoids and the endocannabinoid system as a potential treatment strategy for both early and post-SARS-CoV-19 infection.

Scientific Reports - Assessment of serum parameters caused by the outbreak of mycoplasma pneumoniae pneumonia in children after COVID-19

Sulforaphane (SFN), which is a hydrolysis product from glucoraphanin, a compound found in cruciferous vegetables, has been studied for its potential health benefits, particularly in disease prevention and treatment. SFN has proven to be effective in ...

A growing awareness of the mechanisms by which phytochemicals can influence upstream endogenous cellular defence processes has led to intensified research into their potential relevance in the prevention and treatment of disease. Pharmaceutical ...

Nordic countries maintain population-based registries that have been used to quantify long-term impacts of COVID-19. Here, the authors conduct a systematic review including studies from Sweden, Denmark and Norway on incidence of post-COVID condition, associated healthcare use, sick leave, and new onset diseases.

This cohort study investigates the association between booster vaccinations containing the JN.1 lineage and 29 serious adverse events in Denmark.

This review considers that many organs other than the lungs are affected by COVID-19. Early research largely concentrated on lung damage, although new information indicates that the virus damages at least ten primary body systems: cardiovascular, neurological, renal, hepatic, endocrine, hematological, gastrointestinal, immune and mental health. The author considers clinical trials, pathology, imaging results and biomarker investigations published by mid-2022. Common abnormalities include endothelial dysfunction, chronic inflammation, cytokine storms and microvascular damage, all of which contribute to the pathogenesis of the disease in the entire body. In this article, mild infections may lead to severe conditions including but not limited to myocarditis, brain fog, kidney disorders or immune system burnout. It also examines existing and emerging treatments-antifibrotics, immune modulators and vascular-targeted therapies-and demands a standardized approach to monitoring and management of patients on a long-term basis. This review highlighting that COVID 19 is a long-term systemic disease that requires a multidisciplinary approach.

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Scientific Reports - Inflammatory, fibrotic and endothelial biomarker profiles in COVID-19 patients during and following hospitalization

Translational Psychiatry - Neuroimaging insights into the psychosocial impact of the COVID-19 pandemic: a systematic review

Langfristige gesundheitliche Auswirkungen von COVID-19 bei Kindern Eine neue Studie mit dem bislang umfassendsten metabolischen Profil einer pädiatrischen SARS-CoV-2-Infektion zeigt, dass „trotz typischerweise milderer Symptome während einer akuten COVID-19-Infektion die …

NIH-funded study focused on original virus strain, unvaccinated participants during pandemic.

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Long COVID presents complex symptoms without clear diagnostic criteria, challenging traditional medical understanding and emphasizing the need for compassionate care.

SARS-CoV-2 induces amyloid-β pathology in the central nervous system.

This article after additional peer review at Medical Review and subsequent changes is now also published at https://doi.org/10.1515/mr-2024-0030 Introduction Symptomatic Long COVID affects 10-30% of the COVID-19-infected population depending on what symptoms are measured. (1-3) Organ damage might affect over 50% of post-COVID-19 individuals (4-6) and perhaps more in adolescents and children. (7) As COVID-19 continues … Continued

A new study reveals that the SARS-CoV-2 spike protein remains in brain-protective tissues and skull bone marrow for years after infection, potentially driving long COVID's neurological symptoms.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the COVID-19 pandemic. After the success of therapeutics and worldwide vaccination, the long-term sequelae of SARS-CoV-2 infections are yet to be determined. Common symptoms of COVID-19 include the loss of taste and smell, suggesting SARS-CoV-2 infection has a potentially detrimental effect on neurons within the olfactory/taste pathways, with direct access to the central nervous system (CNS). This could explain the detection of SARS-CoV-2 antigens in the brains of COVID-19 patients. Different viruses display neurotropism that causes impaired neurodevelopment and/or neurodegeneration. Hence, it is plausible that COVID-19-associated neuropathologies are directly driven by SARS-CoV-2 infection in the CNS. Microglia, resident immune cells of the brain, are constantly under investigation as their surveillance role has been suggested to act as a friend or a foe impacting the progression of neurological disorders. Herein, we review the current literature suggesting microglia potentially been a susceptible target by SARS-CoV-2 virions and their role in viral dissemination within the CNS. Particular attention is given to the different experimental models and their translational potential. Keywords: SARS-CoV-2 COVID-19 Microglia CNS Neuroinflammation

Scientific Reports - Remodeling of intracellular architecture during SARS-CoV-2 infection of human endothelium

VIRGINIA (DC News Now) — Imagine being able to walk into a crowded store, restaurant or even movie theater and be able to detect if there’s COVID-19 in the air. It could be a reality in just a few years as a team at Virginia Tech is developing what is essentially a portable rapid test […]

IntroductionLong COVID is a debilitating condition that lasts for more than three months post-infection by SARS–CoV–2. On average, one in ten individuals inf...

Opinion: Kevin Kavanagh, MD, examines a summary of studies on how COVID-19 may damage the brain's frontal lobes, alter personality traits and cognitive functions, and potentially reshape society's dynamics.

Medical News: The Overlooked Culprit Behind Lingering Symptoms Emerging scientific evidence is now pointing to a new root cause behind Long COVID and the growing wave of chronic health problems seen after COVID-19 infection — mitochondrial damage. According to a comprehensive study by researchers from the University of Copenhagen’s Department of Biomedical Sciences, the Copenhagen Uni...

npj Metabolic Health and Disease - Mitochondrial dysfunction in acute and post-acute phases of COVID-19 and risk of non-communicable diseases

SARS-CoV-2 has been reported to potentially remain in the lower respiratory tract for some time after it is no longer detectable in the upper respiratory tract, and this could be a source of reactivation. Reactivation of latent viral infections, such as cytomegalovirus and Epstein-Barr virus, after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is often a clinical problem. COVID-19 is caused by SARS-CoV-2 infection and has a high mortality rate in allo-HSCT recipients. However, little is known about SARS-CoV-2 reactivation following allo-HSCT. In this report, a patient with severe aplastic anemia first developed mild COVID-19 (day 0) with negative antigen test results on day 27. Three months later (day 97), the patient underwent allo-HSCT. Two months post-transplantation (day 157, i.e., five months after the initial infection), the patient developed rapidly progressive respiratory failure and was diagnosed with severe COVID-19. Since the patient was hospitalized and there was no obvious route of infection, we have concluded that reactivation of SARS-CoV-2, which had infected the patient five months earlier, occurred under an immunosuppressive state after allo-HSCT. Regarding allo-HSCT in patients who have previously developed COVID-19, careful monitoring using real-time reverse transcriptase-polymerase chain reaction (RT-PCR) to detect SARS-CoV-2 could be useful for detecting SARS-CoV-2 reactivation and providing early treatment to prevent fatal COVID-19.