The molecular biology of SARS-CoV-2 pathogenesis, host genetics and
associated interactions in infection
Abstract
This new human pathogenic coronavirus belongs to lineage B
betacoronaviruses, taking into account its genome. The SARS-CoV-2 genes
code for the structural and non-structural proteins used throughout
their life cycle and pathogenesis. These proteins govern the functional
characteristics of SARS-CoV-2 infection and its association with host
proteins in pathogenesis. These open new horizons in the battle
virus/host and provide a better understanding of COVID-19 infection.
These understandings are revealed by transcriptome-wide and genome-wide
analyses showing viral and host crosstalk from viral entry to disease
development. It also discloses the acquaintance about antiviral immunity
against SARS-CoV-2 and disease severity. The most crucial event is the
combat between the virus and the host’s antiviral immunity. Based on
insight into immunopathogenesis and pathology, potential susceptibility
genes are involved in immune dysregulation, auto-inflammation, or
autoimmunity mechanisms. This paper addresses host susceptibility,
considerations of immune responses, and the use of these prospects for
antiviral therapeutic leads. Significant interactions between SARS-CoV
infection and host antiviral pathways address innate immune signaling,
which can be a crucial genetic determinant in analyzing COVID-19
susceptibility and disease outcomes. The susceptibility of individuals
is highly associated with genetics and genetic variants, and their
frequencies cause the deviation in the patient vulnerability, which
further decides the clinical condition of viral infection in patients.
These associations provided relationships among host and viral genes
that uncover hidden aspects of giving insights into the vaccine design
and antiviral treatment strategies.