The interindividual variations in the capacity of transforming growth factor-β1 (TGF-β1) production have been ascribed to genetic polymorphisms in TGF-β1 gene. As pathogenesis of HBV has a genetic background, this preliminary study was designed to assess the impact of TGF-β1 (T29C) on the susceptibility of Egyptians to HBV infection. Genotyping was performed using single stranded polymorphism-polymerase chain reaction (SSP-PCR) in 65 Egyptian hepatitis B patients and 50 healthy controls. TGF-β1 plasma levels were measured using Enzyme-linked immunosorbent assay (ELISA). The frequency of CC genotype was significantly higher ( ) in HBV patients compared to controls. On the contrary, TC genotype did not show significant difference in both groups. TT genotype was significantly higher ( ) in controls than HBV patients. Our current preliminary data revealed that the frequency of the genotypes in the controls were within Hardy-Weinberg equilibrium (HWE) while the patients group was out of HWE ( ). TGF-β1 was significantly ( ; ) deceased in the sera of patients as compared to normal subjects. Depending on our preliminary work, CC genotype may act as a host genetic factor in the susceptibility to HBV infection in Egyptians. Taken together, the current data pointed to the importance of polymorphism of TGF-β1 gene (T29C) in HBV infection. 1. Introduction Hepatitis B virus infection (HBV) is a worldwide problem and it is still the main factor of developing chronic HBV, cirrhosis, and hepatocellular carcinoma (HCC), especially in developing countries [1]. There are about 400 million carriers of HBV infection worldwide and over 1 million deaths occur each year as a consequence of fulminant hepatic failure, cirrhosis, and hepatocellular carcinoma [2]. Moreover, 5–10% of infected individuals cannot clear the infection, which leads to a chronic carrier state with or without liver disease chronic [3]. The interaction of the host immune response with HBV, the impact of this interaction on the clinical outcome, and the factors of viral persistence are not yet fully understood. Host genetic factors have been reported to be critical factors which affect the natural history of liver diseases [4]. Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine that regulates cell growth, proliferation, and differentiation [5]. It is produced by several cell types, including monocytes, macrophages, endothelial cells, and vascular smooth muscle cell [6, 7] and it is also produced from a variety of liver cell populations including HSCs, hepatocytes, and LSECs in addition to
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