A shocking third species emerged from a family of coronaviruses (CoV) in late 2019 following viruses causing SARS (Severe Acute Respiratory Syndrome-CoV) in 2003 and MERS (Middle East Respiratory Syndrome-CoV) in 2012; it’s a novel coronavirus now called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; formerly called 2019-nCoV). First emerging in China, it has spread rapidly across the globe, giving rise to significant social and economic costs and imposing severe strain on healthcare systems. Since many attempts to control viral spread has been futile, the only old practice of containment including city lockdown and social distancing are working to some extent. Unfortunately, specific antiviral drugs and vaccines remain un available yet. Many factors are encountered to play essential roles in viral pathogenesis. These include a broad viral-host range with high receptor binding affinity to various human tissues, viral adaptation to humans, a high percentage of asymptomatic but infected carriers, prolonged incubation, and viral shedding periods. There are also a wide variety of pulmonary and extrapulmonary tissue damage mechanisms including direct cell injury or immune-mediated damages involving the immune cells, upregulation of proinflammatory cytokines, and antibody dependent enhancement that can result in multi-organ failure. In this article, we summarise some evidence on the various steps in SARS-CoV-2 pathogenesis and immune evasion strategies to assess their contribution to our understanding of unresolved problems related to SARS-CoV-2 prevention, control, and treatment protocols.
