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1.
Open Access Macedonian Journal of Medical Sciences ; 10:1818-1826, 2022.
Article in English | EMBASE | ID: covidwho-2066696

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome has led to a pandemic of coronavirus disease 2019 (COVID-19). Malnutrition either biochemically or anthropometrically is a well-known risk factor for COVID-19 and may be the vice versa AIM: The objectives of this study were to investigate the prevalence of malnutrition in children infected with COVID-19 through evaluating the nutritional biomarkers such as serum electrolytes, serum albumin, and hemoglobin together with the anthropometric assessment. METHODS: A cross-sectional study that was conducted at El-Matria Teaching Hospital for all children admitted with confirmed COVID-19 for 6 months from February 1, 2021 to the end of July, 2021. Nutritional biochemical evaluation included serum electrolytes particularly the potassium and other nutritional biomarkers such as serum albumin and hemoglobin. Nutritional anthropometric evaluation depended on body mass index, the height/length, weight for length, and weight for height. The prevalence of malnutrition esp. hypokalemia was the main outcome. RESULTS: Hypokalemia was present in 21.8% of the study participants. Other nutritional biomarkers were found as hyponatremia, hypocalcemia, hypophosphatemia, and hypomagnesemia were detected in 49.1%, 38.2%, 21.8%, and 34.5% of the study subjects, respectively. Anthropometric malnutrition was present in most of the enrolled children with COVID-19 in the study (65.5 % [n = 36]) through which overweight and obese children occupied a greater percentage. CONCLUSION: Malnutrition either biochemically or anthropometrically could be linked to COVID-19 in children. COVID-19 could have negative outcomes on the nutritional status such as electrolytes disturbances. Both malnutrition and COVID-19 are considered synergistic associations.

2.
Topics in Antiviral Medicine ; 30(1 SUPPL):9, 2022.
Article in English | EMBASE | ID: covidwho-1880599

ABSTRACT

Background: Life threatening thrombotic events involving both the arterial and venous systems are prominently present in SARS-CoV-2 infected individuals presenting with severe COVID-19. Abnormal clotting also occurs in asymptomatically or mildly infected individuals and in people experiencing post-acute sequelae of SARS-CoV-2 infection (PASC). Clinical management of this clotting disorder has proven difficult in part because these fibrin clots are highly resistant to plasmin-mediated fibrinolysis. Methods: An array of different binding, biochemical, microscopic, and in vivo assays were performed in these studies. All experiments were performed at least three times in triplicate and reported differences were shown to be statistically significant. Results: We find that SARS-CoV-2 Spike directly binds to the terminal clotting factors, fibrinogen and fibrin (Kd of 5.3 μ M and 0.4 μ M respectively). Mixing Spike and plasma accelerates fibrin polymerization. Scanning electron microscopy reveals an abnormal clot structure with finer, denser, and roughened fibrin fibers. Scanning peptide competition assays indicate Spike binds fibrin at three sites: 1) the plasmin cleavage site needed for fibrinolysis;2) a site involved in innate immune signaling via fibrin binding to Complement Receptor 3 (CR3);and 3) a site with no known function. Examination of mice injected 24h earlier with Spike pseudotyped HIV-ΔEnv virions reveals extensive intra-and extravascular fibrin deposition in the lung accompanied by endothelial activation, loss of tight junctions, increased influx of macrophages, and the generation of high levels of reactive oxygen species. This thromboinflammatory response is not observed when Bald virions are injected or when Spike pseudotyped virions are injected into mice lacking fibrinogen. Intriguingly, these Spike-induced proinflammatory effects are blocked by an anti-fibrin monoclonal antibody, 5B8, which interferes with fibrin binding to CR3. Conclusion: Our findings reveal that the SARS-CoV-2 Spike protein binding to fibrinogen/fibrin results in the formation of structurally abnormal, fibrinolysis-resistant blood clots whose inflammatory effects are effectively neutralized by a specific fibrin-targeting monoclonal antibody. While COVID-19 clotting was thought to occur as a result of systemic inflammation, our findings suggest clotting during SARS-CoV-2 infection in fact is a driver of inflammation. Targeting fibrin could lead to novel therapeutic approaches for patients with acute COVID-19 and PASC.

3.
Topics in Antiviral Medicine ; 30(1 SUPPL):64, 2022.
Article in English | EMBASE | ID: covidwho-1880463

ABSTRACT

Background: SARS-CoV-2 primarily infects the lung but may also damage other organs including the brain, heart, kidney, and intestine. Central nervous system (CNS) disorders include loss of smell and taste, headache, delirium, acute psychosis, seizures, and stroke. Pathological loss of gray matter occurs in SARS-CoV-2 infection but it is unclear whether this is due to direct viral infection, indirect effects associated with systemic inflammation, or both. Methods: We used iPSC-derived brain organoids and primary human astrocytes from cerebral cortex to study direct SARS-CoV-2 infection, as confirmed by Spike and Nucleocapsid immunostaining and RT-qPCR. siRNAs, blocking antibodies, and small molecule inhibitors were used to assess SARS-CoV-2 receptor candidates. Bulk RNA-seq, DNA methylation seq, and Nanostring GeoMx digital spatial profiling were utilized to identify virus-induced changes in host gene expression. Results: Astrocytes were robustly infected by SARS-CoV-2 in brain organoids while neurons and neuroprogenitor cells supported only low-level infection. Based on siRNA knockdowns, Neuropilin-1, not ACE2, functioned as the primary receptor for SARS-CoV-2 in astrocytes. The endolysosomal two-pore channel protein, TPC, also facilitated infection likely through its regulatory effects on endocytosis. Other alternative receptors, including the AXL tyrosine kinase, CD147, and dipeptidyl protease 4 (DPP4), did not function as SARS-CoV-2 receptors in astrocytes. SARS-CoV-2 infection dynamically induced type I, II, and III interferons, and genes involved in Toll-like receptor signaling, MDA5 and RIG-I sensing of double-stranded RNA, and production of inflammatory cytokines. Genes activating apoptosis were also increased. Down-regulated genes included those involved in water, ion and lipid transport, synaptic transmission, and formation of cell junctions. Epigenetic analyses revealed transcriptional changes related to DNA methylation states, particularly decreased DNA methylation in interferon-related genes. Long-term viral infection of brain organoids resulted in progressive neuronal degeneration and death. Conclusion: Our findings support a model where SARS-CoV-2 infection of astrocytes produces a panoply of changes in the expression of genes regulating innate immune signaling and inflammatory responses. Deregulation of these genes in astrocytes produces a microenvironment within the CNS that ultimately disrupts normal neuron function, promoting neuronal cell death and CNS deficits.

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