PMC:7253235 / 24625-27612 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7253235","sourcedb":"PMC","sourceid":"7253235","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7253235","text":"Coronavirus Structure and Foundation for Treatment Strategies\nCoronaviruses are a large collection of single-stranded enveloped, non-segmented positive-sense RNA viruses that fall within the family of Coronaviridae and the order nidovirales [55]. Six specific coronaviruses have been identified as human-susceptible, among which alpha and beta subsets demonstrated lower pathogenicity and caused milder respiratory symptoms respectively. Genomic analysis of SARS-COV-2 showcased 96.2% shared sequencing with bat CoV RATG13, thus positing that the bat variant served as the natural host of the virus [4]. However, the severe acute syndromes belong to the B-genus, with envelope-anchored spike protein mediating viral entry into host cells by first binding to a host receptor and subsequently fusing membranes [56]. The COVID-19 infection has a well-defined capsular structure with 14 binding residues, with 8 conserved from prior SARS-CoV infections. The viral genome contains several open reading frames, with majority of the viral RNA-encoding non-structural proteins (NSPs) that play a role in the pathogenesis of disease. Recent research studies focusing on NSP2 and NSP3 demonstrated an in vivo role that these subunits may play in infectious capability and differentiation of COVID-19 [57].\nMechanistically, COVID-19 is found to be linked to Angiotensin-Converting Enzyme 2, a membrane-bound aminopeptidase highly expressed in lung, intestinal, and heart tissue. Beyond being implicated in hypertension and diabetes, ACE-2 further functions as a receptor for coronaviruses [58•]. COVID-19 translocates into lung parenchyma via damaging epithelial cells, resulting in respiratory symptoms, with symptom severity worsening in patients with cardiovascular disease. ACE2 secretion is noted to be elevated in CVD patients due to increased reliance on angiotensin-receptor blockers for management of hypertension. At the receptor level, the receptor-binding domain of SARS-CoV spike protein specifically recognizes ACE2, which contributes to both cross-species and human-to-human transmission [59, 60]. Documented variability is demonstrated between various strains of SARS-CoV in terms of binding affinity and viral attachment, which is preserved across both humans and animal models of disease transmission [61]. The preserved domains across MERS/SARS may contribute to the heightened inflammatory response and cytokine milieu that leads to severe pneumonia [62].\nOn a molecular level, specific associations and descriptive characteristics of the patients identified cytokine abnormalities in ICU-level patients versus non-ICU–level admissions. Compared with non-ICU patients, ICU patients had higher plasma levels of IL-2, IL-7, IL-10, G-CSF, IP-10, MCP-1, MIP-1A, and TNF-a [63•]. Though this cytokine thumbprint is being linked to COVID-19 infection, ARDS similarly showcases elevations in inflammatory markers, questioning origin and role of virally mediated hyperinflammation 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