Covid19-Sources

SARS-CoV-2 infections in children lead to symptoms from mild respiratory illness to severe postacute sequelae of COVID-19, including multisystem inflammatory syndrome in Children (MIS-C). We conducted a metabolic profiling of 147 children’s serum samples, including acute COVID-19 patients, MIS-C patients, and healthy controls. Using nuclear magnetic resonance spectroscopy and liquid chromatography–mass spectrometry, we measured 1101 metabolites. The results revealed distinct metabolic profiles in acute COVID-19 and MIS-C patients, with significant alterations in lipid classes. Both conditions exhibited an elevated Apo-B100/Apo-A1 ratio and increased serum inflammatory markers. MIS-C patients showed unique disruptions, including increased triglycerides and altered lipoprotein composition. Despite milder clinical respiratory symptoms, children’s metabolic disturbances mirrored those seen in severe adult COVID-19 patients, indicating a shared inflammatory response to SARS-CoV-2. This suggests potential long-term health impacts, underscoring the need for continued research into the metabolic consequences of COVID-19 in children.

Background: Coronavirus Disease 2019 has been associated with dysfunction in multiple endocrine organs, including the thyroid gland. While evidence suggests SARS-CoV-2 may influence thyroid function and promote oncogenesis through inflammation and cytokine storms, its role in thyroid cancer remains unclear. This study investigates whether COVID-19 is associated with an increased risk of thyroid cancer development. Methods: We conducted a retrospective cohort study using the TriNetX global federated health research database, encompassing data from 151 healthcare organizations. Adult patients with confirmed COVID-19 between 1 December 2019 and 31 December 2023, were included and compared to a matched cohort without COVID-19. Patients with prior thyroid cancer history or who had received COVID-19 vaccination were excluded in both groups. Propensity score matching (1:1) was performed for age, gender, and overweight/obesity status. The primary outcome was that new-onset thyroid cancer was diagnosed at least one year after COVID-19 diagnosis. Hazard ratios were calculated using Cox proportional hazards models, and subgroup analyses were performed based on age, gender, thyroid function status and treatment modalities. Results: After matching, a significantly higher thyroid cancer incidence was observed between the post-COVID and non-COVID groups. Subgroup analysis revealed a significantly higher risk of thyroid cancer development following COVID-19 diagnosis in patients who developed hyperthyroidism (HR 2.14, 95% CI: 1.04–4.46) or hypothyroid-ism (HR 1.83, 95% CI: 1.12–2.97) compared with the non-COVID population. Male patients also exhibited a higher risk of thyroid cancer after COVID-19 (HR 1.22, 95% CI 1.02–1.46). For patients with hyperthyroidism or hypothyroidism, those who had prior COVID-19 exhibited a relatively higher risk of developing thyroid cancer than those without a history of COVID-19 (HR 4.387, 95% CI: 2.08–9.24 for hyperthyroidism; HR 2.58, 95% CI: 1.58–4.22 for hypothyroidism). Conclusions: Patients with COVID-19 exhibited an increase in thyroid cancer risk, with specific subgroups—male adults and those with post-infectious thyroid dysfunction—also exhibiting increased risk. These findings suggest a potential relationship between SARS-CoV-2 and thyroid oncogenesis, warranting further prospective research.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and Long Covid-19 (LC-19) are complex conditions with no diagnostic markers or consensus on disease progression. Despite extensive research, no in vitro model exists to study skeletal muscle wasting, peripheral weakness, or potential therapies. We developed 3D in vitro skeletal muscle tissues to map muscle adaptations to patient sera over time. Short exposures (48 H) to patient sera led to a significant reduction in muscle contractile strength. Transcriptomic analysis revealed the upregulation of protein translation, glycolytic enzymes, disturbances in calcium homeostasis, hypertrophy, and mitochondrial hyperfusion. Structural analyses confirmed myotube hypertrophy and elevated mitochondrial oxygen consumption In ME/CFS. While muscles initially adapted by increasing glycolysis, prolonged exposure (96–144 H) caused muscle fragility and weakness, with mitochondria fragmenting into a toroidal conformation. We propose that skeletal muscle tissue in ME/CFS and LC-19 progresses through a hypermetabolic state, leading to severe muscular and mitochondrial deterioration. This is the first study to suggest such transient metabolic adaptation.

Erlangen - Viele hatten darauf gehofft, nun meldet das Team um Oberärztin Bettina Hohberger aus Erlangen einen ersten Erfolg: Eine Studie zeigt, dass das Medikament BC007 gegen chronische Erschöpfung nach einer Corona-Infektion helfen kann.

Scientific Reports - Validation of the age, neutrophil to lymphocyte ratio, C reactive protein score on 28 day mortality in the National COVID cohort collaborative

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.

Dabei wollte sie einfach nur leben ...

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 […]