ABSTRACT
In 2002, a severe-to-fatal respiratory disease began in China and was named severe acute respiratory syndrome (SARS). The causative agent was soon found to be a coronavirus and was named SARS-coronavirus (SARS-CoV). Infection was traced to contact with live palm civet cats or raccoon dogs in live animal food markets (“wet markets”) and later, person-to-person. Visiting these markets or restaurants housing these animals before preparing them for customer consumption were among the risk factors for infection in addition to frequent use of taxis and comorbidities. After its initial appearance, SARS spread rapidly through parts of Asia and then to countries around the world before almost completely disappearing in 2003. It caused 8096 cases and 774 deaths. SARS-CoV is a betacoronavirus linage B. The single-stranded RNA genome of coronaviruses is the largest among RNA viruses. The size of the genome, the inaccuracy of replication in most coronaviruses, and homogenous and heterogenous genetic recombination contribute to the high frequency of mutation. The viral spike (S) protein binds to angiotensin-converting enzyme 2 on the host cell before entry. Mutations in the S protein make a substantial contribution to viral transmission to additional host species and cell types in addition to viral virulence as the virus adapted to its new hosts. Interestingly, SARS-CoV isolates from the initial stages of the 2002–2003 epidemic were more virulent than those isolated later and are associated with a 29-nucleotide deletion in the S protein gene. Several insectivorous Chinese bats appear to serve as reservoir hosts for the ancestorial coronavirus. New forms of protection against infection were implemented in China and some other countries and include wearing face masks, thermal screening, and avoiding travel in taxis and public transportation. Their effectiveness in decreasing transmission and the rapid end of the epidemic is unknown.