Pathogenesis and mutagenesis of SARS-CoV-2: cellular attachment, entry, and infection

Coronavirus disease 2019 (COVID-19) is a highly infectious disease characterized by higher leukocyte numbers, acute respiratory distress, and elevated levels of plasma proinflammatory cytokines. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the causative agent of COVID-19, begins its pathogenesis by the binding of the virus to the host's angiotensin-converting enzyme 2 (ACE-2) receptor and then replication. The various replicated viruses then reinfect other cells and organs with ACE-2 receptor and further wreak havoc and could later result in multisystem organ failure. Presently, efforts are on the way to develop vaccines and drugs for this virus. But the current spike in COVID-19 cases linked to mutation in the virus genome and those of its enzymes is a cause of concern. Studies conducted by some authors have identified 6 major clads (basal, D614G, L84S, L3606F, D448del, and G392D), out of which D614G (a G-to-A base change at position 23403 in the Wuhan reference strain) was found to be the most reoccurring clad. This chapter examines all of these.