Molecular Pathogenesis of Human Coronaviruses of 21st Century

Coronaviruses affect both humans and animals, causing respiratory, enteric, hepatic, and neurological diseases. Until the outbreak of severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002, coronaviruses were known to cause very mild infections in humans. However, the ongoing novel coronavirus disease (COVID- 19) that emerged in December 2019 from Wuhan, Hubei province, China, is several folds critical than the disease caused by its predecessors, SARS and MERS coronaviruses of 2002 and 2012, respectively. The evidence shows that all the human coronaviruses of this century, including the ongoing pandemic SARS-CoV-2, were the result of zoonosis, crossing the animal species barrier, causing high morbidity and mortality in the human population. A large number of studies have provided an understanding of earlier SARS-CoV and MERS-CoV induced pathogenesis and host immune response. Immunopathogenesis of current SARS-CoV-2 has also been reported to a significant extent since its emergence. It is evident from the studies reported to date that all the above three human coronaviruses share similarities with respect to clinical symptoms caused, pathological conditions induced, and host immune response that leads to the disease progression to a larger extent. However, certain pathological features associated with SARS-CoV-2 infection are distinct and fatal from the features caused by the other two human coronaviruses. This chapter focuses on the studies related to immune response, molecular pathogenesis of all three human coronaviruses with an emphasis on SARS-CoV-2 and the immune evasion strategies stimulated by individual viral proteins and their driven mechanisms.

Keywords: ACE2, ARDS, COVID-19, Immune Evasion, Immune Response, MERS, Pathogenesis, Pneumonia, SARS-CoV, SARS-CoV-2.