Over time, there may be seroconversion as defined by a loss of HBeAg and development of anti-HBe. Seroconversion is usually preceded by a marked decrease in serum HBV-DNA. Seroconversion may be associated with a flare in serum ALT levels but these levels typically decrease and ABT-199 1257044-40-8 normalize after seroconversion. To decrease the bias of age and gender on the effect of estimates, we conducted multivariable logistic regression analysis and the association between rs430397 and the progression of HBV infection remained significant. Among multiple parameters evaluating liver function, ALB is quantitatively the most important of several plasma proteins formed in the liver. Accordingly, measurement of total concentration of ALB is a useful test of hepatic synthetic function. The relatively long half-life of ALB makes the albumin level a better index of severity and prognosis in patients with chronic liver disease such as LC. And also, these diseases are the common cause of impaired coagulation which was reflected by prolonged PT. In patients with HBV-related LC, we found patients carrying AA genotype had relatively lower ALB levels and higher PTs compared with those carrying GG genotype. This fact further supports the potential association of rs430397 with the outcome of HBV infection. Increasing evidence demonstrated that HBV infection is associated with oxidative stress, which also may cause structural damage to DNA or impede DNA repair process. The preS proteins are retained in the endoplasmic reticulum and subsequently induce ER stress, leading to the expression of ER chaperone GRP78. Accumulation of GRP78 induces ER stress signaling pathway, including unfolded protein response and ER overload response. In addition, cells infected by viruses are usually killed by a variety of reactive oxygen species, which are produced by Kupffer and inflammatory cells. Unfortunately, through these defense mechanisms, oxidative stress may become inevitable and result in oxidative damage to DNA or other macromolecules. Chronic inflammation caused by HBV induced the release of free radicals, cytokines and chemokines resulting in cell proliferation, DNA damage, fibrosis and angiogenesis, and frequently associated with increased hepatocarcinogenesis risk. Cirrhosis may also indicate pathological and genetic changes throughout the liver leading to a field cancerization effect, which increases the risk of hepatocarcinogenesis. GRP78 pathway is one of the most important responders to disease-associated stress. Therefore, rs430397 polymorphism of GRP78 gene in the present study might be owing to, at least partially, genetic instability induced by HBV-related cirrhosis. Our study was limited by the small number of patients, but there would be some concern over the ethics of enrolling further large numbers of patients who were follow-up information on patient survival outcomes.