2020
DOI: 10.1016/j.fct.2020.111769
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Abstract: Common manifestations of COVID-19 are respiratory and can extend from mild symptoms to severe acute respiratory distress. The severity of the illness can also extend from mild disease to life-threatening acute respiratory distress syndrome (ARDS). SARS-CoV-2 infection can also affect the gastrointestinal tract, liver and pancreatic functions, leading to gastrointestinal symptoms. Moreover, SARS-CoV-2 can cause central and peripheral neurological manifestations, affect the cardiovascular system and promote rena… Show more

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Cited by 126 publications
(113 citation statements)
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References 222 publications
(282 reference statements)
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“…Further “hot topics” are the characterization of the effects of antiviral therapies (such as remdesivir), steroids (including dexamethasone), immunomodulatory medications (e.g., anti-interleukin-6), monoclonal antibodies, and anticoagulant agents on the brain [ 119 ]. Since therapeutic responses to COVID-19 vastly differ among centers, the understanding of how the different treatment options during hospitalization and after discharge might be responsible for the variability in both acute and long-term neurological manifestations and their histopathological correlates [ 121 ] remains. Regarding long-term sequelae, neuropathological findings in COVID-19 survivors are totally unstudied.…”
Section: Resultsmentioning
confidence: 99%
“…Further “hot topics” are the characterization of the effects of antiviral therapies (such as remdesivir), steroids (including dexamethasone), immunomodulatory medications (e.g., anti-interleukin-6), monoclonal antibodies, and anticoagulant agents on the brain [ 119 ]. Since therapeutic responses to COVID-19 vastly differ among centers, the understanding of how the different treatment options during hospitalization and after discharge might be responsible for the variability in both acute and long-term neurological manifestations and their histopathological correlates [ 121 ] remains. Regarding long-term sequelae, neuropathological findings in COVID-19 survivors are totally unstudied.…”
Section: Resultsmentioning
confidence: 99%
“…Most patients with a severe form of COVID-19 have elevated levels of proinflammatory cytokines, including interleukin (IL)-6, IL-1β, as well as plasma monocyte chemotactic protein-1 (MCP-1), interferongamma-inducible protein-10 (IP-10), and granulocyte colony-stimulating factor (G-CSF). It has been proposed that high levels of proinflammatory cytokines may lead to shock as well as respiratory failure or multiple organ failure and several studies to evaluate inflammatory mediators are still ongoing [119]. In some patients with COVID-19, the expression of proinflammatory cytokines by myeloid cells decreased, whereas there were elevated plasma levels of inflammatory mediators, including the extracellular newly identified receptor for advanced glycation endproducts binding protein (EN-RAGE), tumour necrosis factor superfamily member 14 (TNFSF14), and oncostatin-M, which correlated with disease severity and bacterial products increased in human plasma.…”
Section: The Immune System Severely Affected By the Attack Of Sars-cmentioning
confidence: 99%
“…Endothelial damage and neuronal apoptosis can be induced by SARS-CoV-2 infection (Pranata et al, 2020). ACE2 receptors on vascular endothelial cell membrane may participate in regulating blood pressure, which is closely related to stroke (Tsatsakis et al, 2020;Viana et al, 2020). Also, SARS-CoV-2 may cause vascular endothelial damages, facilitating viral invasion into CNS (Baig et al, 2020).…”
Section: Mechanism Of Sars-cov-2 Infectionmentioning
confidence: 99%