Objective. This study investigated the association of the single nucleotide polymorphisms (SNPs) in the FAS and FASL genes with the outcome of hepatitis B virus (HBV) infection. Methods. Blood samples were collected from 116 HBV-infected patients at the Hospital of the Santa Casa de Misericordia Foundation (Belém, PA, Brazil). Seronegative individuals were used as controls. DNA samples were extracted from the leukocytes and assayed using the polymerase chain reaction (PCR) followed by RFLP analysis with restriction endonucleases. Results. The frequencies of the mutant genotypes for -670FAS (GG), Ivs2nt-124FASL (GG), Ivs3nt-169FASL ( T/ T), and -844FASL (TT) were higher in the HBV patients, and the FAS-1377AA genotype was more frequent in the control group; however, the differences between the allele and genotype frequencies were not statistically significant. When the HBV patient population was divided into two groups (inactive carriers and active chronic hepatitis patients), the mutant genotypes were found to be more prevalent in the active chronic hepatitis group with respect to the FAS gene polymorphisms; however, this difference was not statistically significant. Conclusions. The results suggest that the polymorphisms in FAS and FASL genes are not associated with HBV infection or even with the natural history of the infection in the Brazilian Amazon region. 1. Introduction The hepatitis B virus (HBV) is a member of the Hepadnaviridae family and the Orthohepadnavirus genus and shares structural and functional characteristics with other family members, such as tropism for hepatic cells, enveloped viral particles, an incomplete double-stranded DNA genome, and viral replication via reverse transcription [1]. In approximately 3–8% of adults infected with HBV, the immune defense system cannot destroy the infected hepatocytes and the inflammation process (hepatitis) persists. When the virus persists for more than 6 months, the infection is defined as chronic hepatitis and the chance of spontaneous healing is very low. When the HBV infection becomes chronic, it is a significant cause of hepatic cirrhosis and hepatocellular carcinoma (HCC) [2, 3]. In the mid-1990s, Suda and colleagues identified a molecule that initiates the process of programmed cell death (apoptosis). This new molecule was reported to bind to a cell membrane receptor (Fas) encoded by the FAS gene and was termed the Fas ligand (FasL) [4, 5]. The FAS gene is located on human chromosome 10q24.1, contains 9 exons and 8 introns, and encodes a 334-amino acid protein. The Fas receptor is
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