Coronaviruses 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].