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.
