Abstract
Many important questions remain regarding severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the viral pathogen responsible for COVID-19. These questions include the mechanisms explaining the high percentage of asymptomatic but highly infectious individuals, the wide variability in disease susceptibility, and the mechanisms of long-lasting debilitating effects. Bioinformatic analysis of four coronavirus datasets representing previous outbreaks (SARS-CoV-1 and MERS-CoV), as well as SARS-CoV-2, revealed evidence of diverse host factors that appear to be coopted to facilitate virus-induced suppression of interferon-induced innate immunity, promotion of viral replication and subversion and/or evasion of antiviral immune surveillance. These host factors merit further study given their postulated roles in COVID-19-induced loss of smell and brain, heart, vascular, lung, liver, and gut dysfunction.
Highlights
In the midst of the current coronavirus disease-19 (COVID-19) pandemic [1], three baffling questions remain
We examined four Gene Expression Omnibus (GEO) datasets that represent two previous deadly coronavirus outbreaks, Middle East Respiratory Syndrome coronavirus (MERS-CoV) [GSE81852], Severe Acute Respiratory coronavirus 1 (SARS-CoV-1) [GSE1739], a comparison of SARS-CoV-1 with Dhori virus, a member of the orthomyxovirus family that includes the influenza viruses [GSE17400] and lastly, a comparison of SARS-CoV-1 with SARS-CoV-2 [GSE148729]
Given reports of neurological and cognitive impairment as a result of COVID-19 [14], we identified several genes implicated in inflammatory neuronal injury, L1CAM (#15), neurodegenerative disorders, DLG4 (#11), Zika-induced microcephaly, MSI1 (#18), and neurocognitive disorders, ATP1A3 (#24); genes implicated in cardiomyopathy, HMGA1 (#17), lung epithelial injury response, FOXP4 (#4) and inflammatory lung injury, PALM (#27); a regulator of T cell development and antiviral immune responses, EFNB1 (#2), an instigator of T cell exhaustion during chronic viral infections, IL2RB (#34), and a regulator of immunoglobulin secretion from B cells, CPLX2 (#10); and among the protective host genes are those involved in interferon-inducible innate antiviral immune responses, TRIM25 (#7)
Summary
In the midst of the current coronavirus disease-19 (COVID-19) pandemic [1], three baffling questions remain.
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