Aim. To investigate whether HLA class I polymorphisms could influence the clearance of hepatitis B surface antigen (HBsAg) in Qidong Han population. Methods. We genotyped HLA-A, -B, and -C loci of 448 individuals with HBV persistent infection and 140 persons with spontaneous clearance of HBsAg by polymerase chain reaction with sequencing based typing (PCR/SBT). All the individuals were unrelated males enrolled from Qidong Han population and were followed up for 10 years. Results. The frequency of HLA-A*33:03:01G was increased in persistent HBV infection group ( value is 0.028), while frequency of HLA-B*13:01:01G was increased in HBsAg clearance group ( value is 0.0004). Conclusion. These findings suggested that the host HLA class I polymorphism is an important factor in determining the outcomes of HBV infection. 1. Introduction Hepatitis B virus (HBV) infection is a major public health problem. Two billion people are expected to be infected with HBV during their lifetime and about 350 million are estimated to be chronic carriers [1, 2]. Nowadays, there are about 120 million HBV chronic carriers in China [3]. HBV infection can cause broad-spectrum diseases, including chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma [4]. The mechanism of HBV clearance and pathogenesis is not yet clearly defined, but host genetic component is one of the critical contributors, which includes age, sex, immune response, and so forth [5–8]. Therefore, understanding the role of host genetic variability in the pathogenesis of HBV infection will help us to uncover the basis for this viral persistence. Human leukocyte antigen (HLA) is an integral component of the immune response on which majority of host genetic studies have focused. Numerous reports described the associations of highly polymorphic HLA gene with the outcome of a wide range of infectious diseases. It is because antiviral cytotoxic T lymphocytes (CTLs) are believed to play a major role in eradication of infection by virtue of their capacity to identify and kill virus-infected cells through recognition of viral peptides presented by HLA class I molecules [9]. Thus, HLA molecules are considered to govern the pathology of disease, progression, or regression along with the viral and environmental factors. The genes of the HLA locus are located on the short arm of chromosome 6. They are arranged in three clusters: class I, class II, and class III. Many previous studies have shown the associations of certain HLA class I genes with the course of HBV infection, but these associations are inconsistent even
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