Understanding the T cell immune response in SARS coronavirus infection

Janice Oh, Hsueh-Ling; Ken-En Gan, Samuel; Bertoletti, Antonio; Tan, Yee-Joo

Severe acute respiratory syndrome (SARS) first emerged in Guangdong, China in late 2002 1 and infected more than 8000 people in 29 countries across 5 continents. 2 According to the World Health Organization (WHO), the fatality rate of the SARS outbreak was estimated to be 9.6%. Of those infected, healthcare workers and caretakers accounted for the majority. The SARS epidemic was officially controlled by July 2003 after the implementation of strict isolation of patients. Sometime into the epidemic, a novel coronavirus, the SARS coronavirus (SARS-CoV), was identified as the causative agent. [3] [4] [5] Molecular epidemiology showed that at least two strains of SARS-CoV infected the patients in Hong Kong, 6 suggesting that the virus had jumped from animal sources to humans on two separate occasions. Later in 2005, reports from two laboratories identified a virus resident in Chinese horseshoe bats that is genetically similar to the human SARS-CoV, pinpointing the horseshoe bat to be a likely natural reservoir of the SARS-CoV. 7, 8 If this is indeed the case, a reemergence of SARS-CoV cannot be ruled out.