Association Between HLA Gene Polymorphism and the Genetic Susceptibility of SARS Infection

Theoretically, any infectious disease with an infection source, transmission route, and susceptible population is able to infect any population. However, studies of human develop‐ ment history, especially those of infectious disease history, have clearly shown that ethnic and regional differences in susceptibility to some infectious diseases actually exist, even if their infection sources and transmission routes are the same. In terms of the 40 types of new infectious diseases that have occurred worldwide in the past 40 years, the epidemiology of some infectious diseases (including severe acute respiratory syndrome (SARS)) has been dominated by regional/territorial or ethnic oriented infections. Examples, along with the year of first occurrence, include:Ebola hemorrhagic fever caused by Ebola virus (1977), Legion‐ naires' disease caused by Legionella pneumophila (1977), hemorrhagic fever with renal syndrome caused by hantavirus (1977), T cell lymphoma leukemia caused by human T-lymphotropic virus type I (1980), hemorrhagic colitis caused by E. coli O157:H7 (1982), hairy cell leukemia caused by human T-lymphotropic virus type II (1982), and the British BSE (bovine spongiform encephalopathy) that created worldwide shock. Along with the effects of infection sources and transmission routes, the contributions of racial or genetic factors to these regional/territorial diseases are still under discussion. Clearly, these infectious diseases occurred more frequently and with greater severity in certain regions and ethnicities. The SARS outbreak in 2002-2003 spread mainly in Asia, especially in China; the most susceptible populations were mainland and overseas Chinese. These observations lead us to consider the important theoretical and practical topic of the relationship between SARS genetic predisposition and individual clinical onset. However, the sudden disappearance of SARS also left us with many revelations.