Pathophysiology of SARS-nCoV-2

Coronaviruses are positive-stranded RNA viruses with nucleocapsid and are the largest known RNA viruses. Coronaviruses have spike glycoproteins as structural elements composed of two subunits S1 and S2. In SARS-nCoV-2, the S2 subunit contains a transmembrane domain, fusion peptide, and cytoplasmic domain. The spike proteins attach to the receptor of the host cell and the fusion peptide interacts directly with the host cell surface membrane and facilitates merging to form a fusion pore. The viral genome is transferred via this pore. According to current research, a mutation in the spike protein might have occurred in November-2019 leading to its animal-to-human transmission. Based on the currently available literature, the viral infection is capable of producing an excessive immune reaction in the host. This reaction is termed as a cytokine storm. The main mediator of this storm is interleukin-6 (IL-6), which is produced by activated leucocytes. The main role of IL-6 is pro-inflammatory. In cytokine storm, excessive levels of cytokines are released which further activate more immune cells resulting in hyperinflammation. IL-6 is also implicated in the pathogenesis of cytokine release syndrome, which is characterised by multiple organ dysfunction and fever. This might also explain why some people have a severe reaction to coronavirus while others don’t.