Abstract
Severe acute respiratory syndrome-coronavirus (SARS-CoV) is responsible for causing respiratory diseases. Its transmission takes place through saliva droplets. SARS-CoV appeared first in Southern China. It spread quickly across the globe from 2002 to 2003. In the wild, horseshoe bats serve as natural reservoir hosts for SARSCoV. Palm civets show high susceptibility toward SARS-CoV. SARS-CoV gradually mutates on continuous transmission from human to human, animal to animal, and animal to human. These mutational changes can occur in viral proteins, which bind to the angiotensin-converting enzyme2 (ACE2) receptor of the host cell surface and cause infection. The worldwide spread of infection leads to the survival of of fitter, more spreadable variants with enhanced ability to adapt to their host. In this chapter, we discussed the different angles of variation in SARS-CoV and the impact of these variations on viral pathogenicity. During this study, we observed many variations in virus spike protein, variation in amino acid residues, variation in open reading frames, the interaction of spike with host ACE2 receptor, genetic variability with OC43, the impact of the variation in IL-12, RBI, and the variation in serine protease. No proven treatments, cures, or pre-emptive strategies were available for SARA-CoV. Coronaviruses found in bats show genetic diversity, pointing out our poor understanding of viral zoonosis from wild animals. Viral zoonosis can be prevented by considering the concept of “One Health”.
Keywords: SARS-CoV, Foshan, horseshoe bats, palm civets, genetic mutations, genetic diversity, viral zoonosis.