in a lower frequency in chronic patients than in individuals with P = 0.079; OR = 0.40;. In chronic patients with histological alterations it was not observed the genotype TGFB1+869 C/C, against 24.4% in the self limited infection group (100 versus 75.6%; P = 0.096; OR = 7.67; . Further studies in other populations, and evaluation of a greater number of individuals could contribute for a better understanding of the cytokine genetic polymorphism influence in HBV infection evolution. Key words: cytokine gene polymorphism -hepatitis B -genetic associationThe infection by the hepatitis B virus (HBV) appears under different forms of evolution, ranging from the asymptomatic and self-limited infection to the chronic state, which can develop into chronic hepatitis, cirrhosis, and hepatic-cellular carcinoma (Thomas & Strickland 2000). It is estimated that the virus infected 350 million people in the whole world, forming a reservoir which facilitates the spreading of the disease (Kane 1995). Furthermore, in spite of the transmission reduction after the vaccination advent (Shih et al. 1999, BerliozArthaud et al. 2003, the infection remains as an important cause of chronic hepatic disease (Thomas & Strickland 2000).The Health Ministry estimates that 1% of the Brazilian population has chronic diseases related to HBV (Ministério da Saúde 2003, Ferreira 2004. The factors that lead a patient with acute infection by HBV to become persistently infected are not totally established. Environmental factors as well as factors innate to the virus do not completely explain the different forms of the HBV infection evolution (Chu & Lok 2002, Kao et al. 2002, bringing up a discussion of the implication of genetic factors in disease evolution (Thio et al. 1999, Thursz 2001.The initial anti-HBV immune response promotes the killing of infected cells by the virus and the secretion of antiviral cytokines by cells of the innate immunity (Ferrari et al. 2003). However, the infection control is not reached at this stage of HBV response. A vigorous and polyclonal immune response of T cells is pointed out as fundamental for the virus elimination and disease resolution (Guidotti et al. 1999). The well-successful response to HBV is a result of both specific anti-virus cytotoxic T-cells activity, which eliminates the infected cells, and non-cytolitic mechanisms exerted through cytokines released by T and non-T cell infiltrates. The cytokines are able to suppress the viral expression and replication, mediating the infection control without causing death of the infected cell. The evolution of the infection to chronicity is associated to a weak or undetectable humoral immune response, and is identified by the persistency of HBV's surface antigen (HBsAg) in the circulation (Jung & Pape 2002, Ferrari et al. 2003.Several studies have evaluated the influence of genetic factors in the cytokine production by cells of the immune system. The genetic polymorphism was pointed out because it correlates to both the transcription level and in vitro production of tu...