The clinical presentation of chronic hepatitis B virus infection in Asian Americans: a single center retrospective study.

BACKGROUND: The clinical course of chronic hepatitis B virus (HBV) infection varies with ethnicity. Little is known about the clinical presentation of chronic HBV infection in Asian Americans. OBJECTIVES: To define the clinical presentation of chronic HBV infection in Asian Americans. METHODS: This is a retrospective study that used systematic chart review and statistical analysis to investigate 213 Asian-American patients with chronic HBV infection who presented to a university medical center. RESULTS: This cohort included 55.8% male patients, 97.9% were born outside the US, and 52.3% reported a family history of HBV infection. Of the 56 patients with liver biopsy, 34.0% had stage 3 to 4 fibrosis. In patients with available data, 21.5% were hepatitis B e antigen positive [HBeAg (+)] and 31.1% had HBV DNA levels >1 x 10(6) copies/mL. Patients with HBeAg (+) HBV infection were diagnosed at a younger age (P=0.002) and with higher alanine aminotransferase (P=0.001) and HBV DNA (P=0.001) levels. Although only 3.3% presented with obesity (ie, body mass index >or=30 kg/m2), 43.4% had evidence of hepatic steatosis. Presentation of hepatocellular carcinoma was associated with an older age at diagnosis (P<0.001), male sex (P<0.001), tobacco use (P<0.001), a greater degree of fibrosis on liver biopsy (P=0.01), and higher alanine aminotransferase, aspartate aminotransferase (P<0.001), and a fetoprotein (P<0.001) levels. CONCLUSIONS: Chronic HBV infection in foreign-born Asian Americans was characterized by a low rate of HBeAg (+) and male predominance as well as high rates of family history of HBV infection, hepatic fibrosis, and hepatic steatosis.

Coordinate effects of human immunodeficiency virus type 1 protein Tat and cellular protein Puralpha on DNA replication initiated at the JC virus origin.

JC virus (JCV) causes progressive multifocal leukoencephalopathy, a demyelinating disease in brains of individuals with AIDS. Previous work has shown that the Tat protein, encoded by human immunodeficiency virus type 1 (HIV-1), can interact with cellular protein Puralpha to enhance both TAR-dependent HIV-1 transcription and JCV late gene transcription. Tat has been shown to activate JCV transcription through interaction with Puralpha, which binds to promoter sequence elements near the JCV origin of replication. DNA footprinting has shown that Puralpha and large T-antigen cooperatively interact at several binding sites in the origin and transcriptional control region. Overexpression of Puralpha inhibits replication initiated at the JCV origin by T-antigen. In transfected glial cells Tat reversed this inhibition and enhanced DNA replication. In an in vitro replication system maximal activation by Tat, more than sixfold the levels achieved with T-antigen alone, was achieved in the presence of Puralpha. Effects of mutant Tat proteins on both activation of replication and binding to Puralpha have revealed that Cys22 exerts a conformational effect that affects both activities. The origin of an archetypal strain of JCV was less susceptible to activation of replication by Tat relative to the rearranged Mad-1 strain. These results have revealed a previously undocumented role for Tat in DNA replication and have indicated a regulatory role for JCV origin auxiliary sequences in replication and activation by Tat.