Hepatitis B virus genotype G (HBV/G) is a unique genotype of HBV which contains a 36-nucleotide insertion in the Core gene as well as 2 mutations that lead to stop codons in the Pre-Core coding region. Chronic infection with HBV/G is not known to occur without a co-infecting HBV genotype, suggesting that it is defective on its own. This study aims to look at the replication capacity of HBV/G, HBV/A, and HBV/A/G recombinant strains circulating in Canada and to determine the relationship between co-infecting strains. Four full-length HBV genomes were isolated from 2 different patients and transiently transfected into the HepG2 human hepatoma cell line for phenotypic analysis of each strain. HBV/G, HBV/A and HBV/A/G recombinant strains were isolated from Patient 1, while a different HBV/A/G recombinant strain was isolated from Patient 2. HBV replication capacity was measured using a quantitative real time PCR assay. Markers of replication, such as secreted HBsAg and HBeAg, intracellular core particles and replicative DNA intermediates were measured by ELISA, Western blot and Southern blot, respectively. HBV/G demonstrated a higher replicative capability, relative to its co-infecting strains, while both HBV/A/G strains had levels of secreted HBV DNA greater than HBV/A alone, suggesting a modulating effect due to recombination. Replication marker levels revealed possible reasons for a co-infection requirement during HBV/G infection such as HBeAg for chronicity. These observations demonstrate the potential interactions of HBV/G with its co-infecting HBV genotype and provide the first reported phenotypic analysis of a HBV recombinant.

In 2010, the Hepatitis B virus (HBV) infected 1.2 million people in the United States, many of whom were unaware of their infection (CDC, 2010). The available research on HBV infection is predominately among Asian American, Native Hawaiian, and other Pacific Islander. HBV infection and Human Immunodeficiency Virus (HIV) infection share similar modes of transmission. Very little HBV research has been dedicated to the African American females; who accounted for 29% of the new HIV cases among young adolescents in 2010 (CDC, 2010). Due to the common mode of transmission of HIV and Hepatitis B many persons at risk for HIV are also at risk for contracting Hepatitis B. One’s risk for acquisition of HBV can be mitigated or eliminated by vaccination or naturally acquired immunity. In the absence of both, an individual is susceptible to acquisition of HBV. The aims of this study are to define susceptibility of non-Hispanic, blacks to Hepatitis B infection compared to other races as well as defining possible risk factors that may increase or decrease their susceptibility.

Hepatitis B virus genotype G (HBV/G) is a unique genotype of HBV which contains a 36-nucleotide insertion in the Core gene as well as 2 mutations that lead to stop codons in the Pre-Core coding region. Chronic infection with HBV/G is not known to occur without a co-infecting HBV genotype, suggesting that it is defective on its own. This study aims to look at the replication capacity of HBV/G, HBV/A, and HBV/A/G recombinant strains circulating in Canada and to determine the relationship between co-infecting strains. Four full-length HBV genomes were isolated from 2 different patients and transiently transfected into the HepG2 human hepatoma cell line for phenotypic analysis of each strain. HBV/G, HBV/A and HBV/A/G recombinant strains were isolated from Patient 1, while a different HBV/A/G recombinant strain was isolated from Patient 2. HBV replication capacity was measured using a quantitative real time PCR assay. Markers of replication, such as secreted HBsAg and HBeAg, intracellular core particles and replicative DNA intermediates were measured by ELISA, Western blot and Southern blot, respectively. HBV/G demonstrated a higher replicative capability, relative to its co-infecting strains, while both HBV/A/G strains had levels of secreted HBV DNA greater than HBV/A alone, suggesting a modulating effect due to recombination. Replication marker levels revealed possible reasons for a co-infection requirement during HBV/G infection such as HBeAg for chronicity. These observations demonstrate the potential interactions of HBV/G with its co-infecting HBV genotype and provide the first reported phenotypic analysis of a HBV recombinant.

Thesis (Ph. D.)--University of Adelaide, 1986. / Offprints of author's four journal articles in pocket. Includes bibliographical references (leaves 131-147).

Thesis (M. Phil.)--University of Hong Kong, 2008. / Also available in print.

Diss. (sammanfattning) Umeå : Univ., 2004. / Härtill 4 uppsatser.

Thesis (M. Phil.)--University of Hong Kong, 2008. / Includes bibliographical references (leaves 94-113) Also available in print.

Thesis (M.D.)--University of Hong Kong, 1992. / Includes bibliographical references (leaves 251-295).

Thesis (M.D.)--University of Hong Kong, 1991.

Heidelberg, Univ., Diss., 2005.