%0 Journal Article
%T The TNF-¦Á -308 Promoter Gene Polymorphism and Chronic HBV Infection
%A Sirous Tayebi
%A Ashraf Mohamadkhani
%J Hepatitis Research and Treatment
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/493219
%X Background and Aims. TNF-¦Á -308 allele promoter polymorphism has been known to be a potential prognostic factor in patients with chronic HBV infection. We tried to determine how TNF-¦Á -308 allele promoter polymorphism would affect the prognosis in patients with chronic HBV infection. Methods. We searched MEDLINE, EMBASE, and reference lists of relevant review articles related to the association between ¡°TNF-¦Á G-308A promoter polymorphism¡± with ¡°chronic HBV infection¡±. We only focused on searching -308 locus in published studies. We reviewed 21 original articles about TNF-¦Á -308 allele polymorphism and its effect on prognosis in patients with chronic HBV infection and discussed the results. Results. conflicting results were observed. The results were divided into 3 groups including neutral, negative, and positive associations between TNF-¦Á -308 allele polymorphism and prognosis in patients with chronic HBV infection. We summarized the primary data as a table. Conclusions. Authors concluded that although there is an upward trend in evidence to claim that there is a positive relation between TNF-¦Á G-308A promoter polymorphisms and resolution of chronic HBV infection, due to many biases and limitations observed in reviewed studies, an organized well-designed study is needed for clarifying the real association. 1. Introduction It is believed that during chronic hepatitis B infection, the host immune response is responsible for both hepatocellular damage and viral clearance [1, 2]. Hepatocyte damage persuades an inflammatory response through activation of tissue macrophage Kupffer cells [3]. These activated cells secrete antiviral cytokines which is thought to be central in suppression or clearance of HBV from the infected liver [4]. Cytokines are proteins or glycoproteins produced by cells acting on their specific receptors on the other cells¡¯ surfaces. They are central mediators of inflammatory events such as infection or peripheral trauma. Several cytokines have been identified that participate in the process of viral clearance via host immune response to HBV. They include TNF-¦Á, TGF¦Â, PGF, and other factors contributing towards the fibrogenesis [5, 6]. Among these, TNF-¦Á is the most important cytokine in host immune response to viral infection [7, 8]. TNF-¦Á is a pleiotropic cytokine, located 850£¿kb telomeric of class II HLA-DR locus of the short arm of chromosome 6, which induces cellular responses such as proliferation, production of inflammatory mediators, and cell death [9]. In the liver, TNF-¦Á is involved in pathophysiology of viral hepatitis,
%U http://www.hindawi.com/journals/heprt/2012/493219/