Selection Of Key HBV Gene Fragment (S) For Effects On TRAIL-Inducing Apoptosis And Its Molecular Mechanisms

The hepatitis B virus(HBV) is recognized as a major causative agent for acute or chronic hepatitis, liver cirrhosis and even hepatocellular carcinoma, which are worldwide health problems, especially in China. Till now, the pathogenesis for HBV infection is still not clear. But studies showed that imbalanced apoptosis of liver cells induced by HBV infection is not only one of the major causes for liver injury, but also plays an indispensable, even decisive role in the prognosis and regress for patients with HBV infection.Many studies have shown that apoptotic molecules, such as TNFα, FasL, play important roles in liver injury induced by HBV infection. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), originally identified in 1994, is a member of the TNF superfamily. Its most dramastic characteristic is that TRAIL selectively induces apoptosis of tumor cells or virus-infected cells while leaving normal cells intact. Many factors, such as virus/viral protein, radiation, drugs, could affect the sensitivity of target cells towards TRAIL. In previous studies, we firstly demonstrated that infection of HBV enhanced the sensitivity of hepatoma cell line towards TRAIL, which might play a certain role in liver injury induced by HBV. However, there're at least four open reading frames(ORF) in HBV genome, which code corresponding viral proteins. Then, which are the most critical fragment(s) for effects of HBV on TRAIL-induced apoptosis? What key points do these fragments affect in the TRAIL signaling pathway? Therefore, on the basis of these research backgrounds, we firstly developed the study about the mechanisms for effects of HBV on TRAIL-induced apoptosis and made some definitive achievements.