Modulation of host-pathogen dynamics through SARS-COV-2 at gastrointestinal-lung axis

Abstract

SARS-CoV-2, a positive sense enveloped RNA virus, emerged as the reason behind one of the most horrific pandemics in human history, COVID-19. The unusually high infectivity and further pathogenesis in the host worsen the condition. Till October 2023, approximately 700 million cases and 70 million COVID-19 deaths were reported worldwide [1]. In India, 45 million cases and 5 million deaths were reported during this period [1]. SARS-CoV-2 belongs to the family Coronaviridae and genus Betacoronavirus [2]. The virus is one of the largest known RNA viruses with a genome size of ~30kB that encode structural proteins like Spike (S), Envelope (E), Membrane(M), and Nucleocapsid (N), nonstructural proteins NSP1-10 and NSP12-16. Besides these two, the viral genome encodes nine accessory proteins [2]. Most of these proteins have distinct functions and help in viral entry, release, and pathogenesis. The structural proteins S, M, and E help propagate infection in the host cells. Unlike the N protein that is conserved in most variants, S, M, and E proteins have acquired multiple mutations.