The current outbreak of SARS-CoV-2 has raised various clinical and
scientific questions, including the effect of host genetic factors on pathogenesis and
disease susceptibility. MERS-CoV is a highly pathogenic virus in humans, causing
high mortality (30-40%) and morbidity. CoVs are found to be widespread in man,
poultry, and mammals. MERS-CoV enters the host cells by attachment with DPP4
receptors; it hijacks the host cell cycle, which helps in its survival and proliferation.
Understanding the innate immune response against MERS-CoV is essential in the
treatment development and precautionary measures. Nonstructural protein 1 (nsp1) has
attracted greater attention as a potential virulence factor and a possible target for
vaccine development. Downregulation of Th2, inadequate Th1 immune response, and
overexpression of inflammatory cytokines IL-1α IL-1β, and IL-8 occur in the lower
respiratory tract of patients infected with MERS-CoV. Research has shown that high
viral load, high expression of inflammatory cytokines, and the downregulation of Th1
and Th2 response result in severe infection, contribute to lung inflammation, develop
acute respiratory distress syndrome (ARDS) and pneumonia, and cause high fatality.
Keywords: Cell cycle, Genetic, Interleukin, MERS-CoV, Nonstructural protein.
