Severe Acute Respiratory Syndrome in Association with Human leukocyte Antigen and Clinical Implications

Human leukocyte antigen (HLA) is the most polymorphic genetic system in humans, with numerous alleles, and subsequently, various possible combinations [1]. These genes, the products of histocompatibility complex (MHC) [2] are located in the short arm of chromosome 6 at band p 21.3 [2] and are divided into three classes, I, II and III [1]. HLA class I is responsible for coding the molecules HLA-A, -B and -C, present in almost all somatic cells with killing of viral infected targets by class I antigens restrict cytotoxic T-cell (CD8+) function [2] while HLA class II genes code the molecules HLA-DR, -DQ and -DP [1] by presentation of exogenous antigens to T-helper cells (CD4+) or antigen presenting cells (APC) [2]. This polymorphism contributes to the differences in susceptibility to diseases among genetically distinct groups [1]. The molecules coded for by the HLA system are responsible for the antigen presentation [1]. The T lymphocytes that are linked to HLA molecules only recognize antigens by the antigen-specific cell surface receptor-antigens interaction [2], thus the HLA antigens [1] and MCH molecules [2] apparently participate in controlling susceptibility and resistance to various diseases. Some infectious diseases were considered as familial before the finding of the causative microorganism and early twin studies indicated that there was a substantial host genetic influence on susceptibility to diseases such as polio and tuberculosis (TB) [3]. At present, it has been confirmed that human genetic variation demonstrates a major influence on the course of diseases caused by several infectious microorganisms [3].