by Lau Tze Chin, Gene. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references (Leaves 170-195). / Abstract --- p.1 / Acknowledgement --- p.3 / List of tables --- p.4 / List of figures --- p.6 / List of abbreviations --- p.7 / Chapter Chapter One - --- Introduction --- p.9 / Chapter 1.1. --- Historical Aspects --- p.9 / Chapter 1.2. --- Classification of hepatitis B virus --- p.12 / Chapter 1.2.1. --- Hepadnaviruses --- p.12 / Chapter 1.2.2. --- Comparative properties of hepadnaviruses --- p.13 / Chapter 1.2.2.1. --- Physical properties --- p.13 / Chapter 1.2.2.2. --- Genetic relatedness --- p.15 / Chapter 1.2.2.3. --- Pathogenesis --- p.16 / Chapter 1.3. --- Structural and morphological properties of HBV --- p.17 / Chapter 1.4. --- Molecular biology of HBV --- p.20 / Chapter 1.4.1. --- Molecular structure of HBV --- p.20 / Chapter 1.4.1.1. --- Biochemistry of the virion envelope --- p.20 / Chapter 1.4.1.2. --- The nucleocapsid --- p.21 / Chapter 1.4.1.3. --- Structural features of HBV genome --- p.23 / Chapter 1.4.2. --- Genetic organization of HBV --- p.24 / Chapter 1.4.3. --- Infection cycle of HBV --- p.29 / Chapter 1.4.3.1. --- Viral attachment and internalization --- p.29 / Chapter 1.4.3.2. --- Replication of HBV --- p.30 / Chapter 1.4.3.3. --- Gene expression and regulation --- p.31 / Chapter 1.4.3.4. --- Host-virus DNA interaction --- p.33 / Chapter 1.5. --- Epidemiology and transmission of HBV --- p.34 / Chapter 1.5.1. --- World wide prevalence --- p.35 / Chapter 1.5.1.1. --- HBsAg prevalence --- p.35 / Chapter 1.5.1.2. --- Cumulative rate of HBV infection --- p.35 / Chapter 1.5.1.3. --- Age specific pattern of HBV infection --- p.36 / Chapter 1.5.2. --- Epidemiological pattern of HBV in Hong Kong --- p.37 / Chapter 1.5.3. --- Mode of transmission --- p.38 / Chapter 1.6. --- Clinical outcomes of HBV infection --- p.38 / Chapter 1.6.1. --- Acute infection --- p.41 / Chapter 1.6.2. --- Chronic infection --- p.42 / Chapter 1.6.3. --- Primary hepatocellular carcinoma --- p.43 / Chapter 1.7. --- Laboratory diagnosis of hepatitis B --- p.44 / Chapter 1.7.1. --- The HBV markers --- p.47 / Chapter 1.7.1.1. --- HBsAg and anti-HBs --- p.47 / Chapter 1.7.1.2. --- HBcAg and Anti-HBc --- p.47 / Chapter 1.7.1.3. --- HBeAg and anti-HBe --- p.49 / Chapter 1.7.1.4. --- HBV-associated DM polymerase --- p.49 / Chapter 1.7.1.5. --- HBV-DNA --- p.49 / Chapter 1.7.2. --- Methodology in the detection of hepatitis B markers --- p.50 / Chapter 1.7.2.1. --- Direct detection of HBV and HBV antigens --- p.50 / Chapter 1.7.2.2. --- Serological detection of HBV markers --- p.51 / Chapter 1.7.2.3. --- HBV-associated DNA polymerase assay --- p.51 / Chapter 1.7.2.4. --- Molecular technique for the detection and quantitation of HBV-DNA --- p.52 / Chapter 1.8. --- Antiviral therapy in hepatitis B --- p.52 / Chapter 1.8.1. --- Therapeutic agents for treatment of HBV infection --- p.53 / Chapter 1.8.1.1. --- Steroids --- p.53 / Chapter 1.8.2.2. --- Nucleoside analogs --- p.54 / Chapter 1.8.1.3. --- Interferon --- p.55 / Chapter 1.8.2. --- Clinical trials of interferons --- p.55 / Chapter 1.9. --- Extrahepatic tissue tropism of HBV --- p.62 / Chapter 1.10. --- Objective and design of study --- p.65 / Chapter 1.10.1. --- Objectives of study --- p.65 / Chapter 1.10.2. --- Study design --- p.66 / Chapter 1.10.2.1. --- Cross-sectional study --- p.67 / Chapter 1.10.2.2. --- Longitudinal study --- p.67 / Chapter 2.1. --- Materials --- p.71 / Chapter 2.1.1. --- Patients recruitment and clinical materials --- p.71 / Chapter 2.1.1.1. --- Cross-sectional study --- p.71 / Chapter 2.1.1.2. --- Longitudinal study --- p.71 / Chapter 2.1.2. --- Bacteria] stock --- p.71 / Chapter 2.1.3. --- "Chemicals, equipments and consumables" --- p.72 / Chapter 2.1.4. --- Buffers and solutions --- p.72 / Chapter 2.1.4.1. --- Phosphate buffer saline (PBS) --- p.72 / Chapter 2.1.4.2. --- Leucocyte lysis buffer (X 5)(LLB) --- p.72 / Chapter 2.1.4.3. --- Buffer equilibrated phenol (BEP) --- p.76 / Chapter 2.1.4.4. --- Phenol-Chloroform mixture --- p.76 / Chapter 2.1.4.5. --- 3.0M sodium acetate (pH 5.2) --- p.76 / Chapter 2.1.4.6. --- Tris-EDTA buffer (pH 8.0) (TE) --- p.76 / Chapter 2.1.4.7. --- Stock salmom sperm DNA solution --- p.77 / Chapter 2.1.4.8. --- Tracking dye --- p.77 / Chapter 2.1.4.9. --- Tris-borate electrophoresis buffer (TBE) --- p.77 / Chapter 2.1.4.10. --- Luria-Bertani Broth (LB) --- p.77 / Chapter 2.1.4.11. --- Solution ] --- p.78 / Chapter 2.1.4.12. --- Solution ]] --- p.78 / Chapter 2.1.4.13. --- Potassium acetate buffer (pH 5.4) --- p.78 / Chapter 2.1.4.14. --- Column elution buffer (CEB) --- p.78 / Chapter 2.1.4.15. --- NPMEB solution --- p.79 / Chapter 2.1.4.16. --- Neutralizing solution --- p.79 / Chapter 2.1.4.17. --- Standard saline citrate (SSC) --- p.79 / Chapter 2.1.4.18. --- Denhardt solution --- p.79 / Chapter 2.1.4.19. --- Prehybridization solution (PS) --- p.80 / Chapter 2.1.4.20. --- NETFAP Solution --- p.80 / Chapter 2.1.4.21. --- Heparin solution --- p.81 / Chapter 2.1.4.22. --- Hybridization mix for oligo-nucleotide probe --- p.81 / Chapter 2.1.4.23. --- NEPS solution (pH 7.0) --- p.81 / Chapter 2.1.4.24. --- Restriction endonuclease and buffer --- p.82 / Chapter 2.2. --- Methods --- p.82 / Chapter 2.2.1. --- Sample preparations --- p.82 / Chapter 2.2.1.1. --- Isolation of plasma and peripheral blood leucocytes (PBL) --- p.82 / Chapter 2.2.1.2. --- Extraction of DNA from Peripheral blood leucocytes --- p.83 / Chapter 2.2.1.3. --- Quantitation of Peripheral blood leucocyte DNA --- p.83 / Chapter 2.2.2. --- Preparation of radio-labelled HBV-DNA probe --- p.84 / Chapter 2.2.2.1. --- Plating and selection of bacterial stock --- p.84 / Chapter 2.2.2.2. --- Growth of E. coli HB101 and amplification of pAM6 --- p.84 / Chapter 2.2.2.3. --- Harvesting of E. coli and extraction of plasmid pAM6 --- p.84 / Chapter 2.2.2.4. --- Purification of plasmid pAM6 --- p.86 / Chapter 2.2.2.5. --- Large scale isolation and purification of HBV genome from plasmid pAM6 --- p.86 / Chapter 2.2.2.6. --- Radio-labelling of HBV-DNA --- p.88 / Chapter 2.2.2.6.1. --- Nick-translation of total HBV-DNA genome --- p.88 / Chapter 2.2.2.6.2. --- Multi-primer labelling of total HBV- DNA genome --- p.88 / Chapter 2.2.2.6.3. --- End-labeling of 21-base HBV oligo- nucleotide --- p.88 / Chapter 2.2.2.6.4. --- Determination of labelling efficiency --- p.89 / Chapter 2.2.2.7. --- Purification of labelled HBV-DNA probe --- p.90 / Chapter 2.2.2.7.1. --- Total genomic HBV-DNA probe (pAM6 probe) --- p.90 / Chapter 2.2.2.7.2. --- Oligo-nucleotide HBV-DNA probe (oligo probe) --- p.90 / Chapter 2.2.3. --- Hybridization study of clinical samples --- p.91 / Chapter 2.2.3.1. --- Solution hybridization of sera samples --- p.91 / Chapter 2.2.3.2. --- Spot hybridization of sera samples --- p.91 / Chapter 2.2.3.2.1. --- "Pre-hybridization treatment of sera samples (adapted from Lin et al.,1987)" --- p.91 / Chapter 2.2.3.2.2. --- Pre-hybridization and hybridization of the membrane --- p.92 / Chapter 2.2.3.2.3. --- Washing of membrane --- p.92 / Chapter 2.2.3.2.4. --- Final treatment and autoradiography: --- p.92 / Chapter 2.2.3.3. --- Quantitation of HBV-DNA in the sera samples: --- p.93 / Chapter 2.2.4. --- Assay for serological Hepatitis B marker --- p.93 / Chapter Chapter Three - --- Results --- p.93 / Chapter 3.1. --- Preparation of HBV-DNA probes --- p.95 / Chapter 3.2. --- Radiolabelling of HBV-DNA --- p.95 / Chapter 3.3. --- Hybridization methodology --- p.98 / Chapter 3.4. --- Comparison of the performance of HBV-DNA probes --- p.100 / Chapter 3.4.1. --- Quantitation of serum HBV-DNA --- p.100 / Chapter 3.4.2. --- Comparative hybridization performance of different HBV-DNA probes --- p.105 / Chapter 3.5. --- Clinical application of HBV-DNA probe:Detection of HBV-DNAin serum and peripheral blood leucocytes (PBL) --- p.109 / Chapter 3.5.1. --- Cross-sectional study --- p.112 / Chapter 3.5.1.1. --- Frequency of HBV-DNA detection in relation to different clinical manifestations --- p.112 / Chapter 3.5.1.2. --- Frequency of HBV-DNA detection in relation to the serological status --- p.114 / Chapter 3.5.1.3. --- Distribution of serum and PBL HBV-DNA level in chronic hepatitis B patients in relation to the different HBV-related manifestations --- p.119 / Chapter 3.5.2. --- Longitudinal study of patients with chronic hepatitis B under interferon therapy with prednisolone pretreatment --- p.123 / Chapter 3.5.2.1. --- Features of patients under study --- p.123 / Chapter 3.5.2.2. --- Correlation between the occurrence of HBV- DNA and HBeAg in serum --- p.123 / Chapter 3.5.2.3. --- Outcome of clinical trial: --- p.126 / Chapter 3.5.2.3.1. --- Number of patients responding to therapy: --- p.126 / Chapter 3.5.2.3.2. --- Variation in serum HBV markers during the course of study --- p.128 / Chapter 3.5.2.3.3. --- Change of HBV-DNA statusin peripheral blood leucocytes --- p.134 / Chapter Chapter Four - --- Dicussion --- p.140 / Chapter 4.1. --- Preparation of HBV-DNA hybridization probes --- p.140 / Chapter 4.1.1. --- Source of HBV-DNA --- p.140 / Chapter 4.1.2. --- Raidolabelling of HBV-DNA --- p.141 / Chapter 4.2. --- Hybridization methodology --- p.141 / Chapter 4.2.1. --- Optimization of hybridization conditions --- p.141 / Chapter 4.2.2. --- Comparison of the performance among different HBV- DNA probes --- p.144 / Chapter 4.3. --- Detection of HBV-DNA in clinical serum samples --- p.148 / Chapter 4.3.1. --- Crossectional study of patients with various categories of HBV related diseases --- p.148 / Chapter 4.3.1.1. --- HBV-DNA detection in serum --- p.148 / Chapter 4.3.1.2. --- Detection of HBV-DNA in peripheral blood mononuclear cells --- p.153 / Chapter 4.3.2. --- Longitudinal studies of patients undergoing antiviral therapy --- p.159 / Chapter 4.3.2.1. --- Serum HBV-DNA and HBeAg --- p.159 / Chapter 4.3.2.2. --- HBV-DNA in peripheral blood leucocytes --- p.163 / Conclusion --- p.166 / Future perspectives --- p.168 / References --- p.170

ABSTRACT In sub-Saharan Africa a causal relationship has been established between hepatitis B virus (HBV) infection and membranous nephropathy (MN), especially in Black children. The most common method of treatment is interferon therapy, which is however, only effective in 30-40% of patients. The reason for this is unclear. The objective of this pilot study was to determine whether mutations in the complete surface gene of HBV isolated from Black children with HBV-associated MN before, during and after treatment with interferon, had any effect on treatment response and vice versa. HBV DNA was extracted from the serum of a responder, reverter and non-responder patient before, during (4 and 16 weeks) and after (40 weeks) IFN treatment. The preS1/preS2/S region was amplified and cloned, and the clones sequenced. Sequence analyses revealed the preS2 region to be the most variable in the reverter and non-responder and HBsAg was the most variable in the non-responder. Phylogenetic analysis showed that the viral population dynamics between the responder strains and the reverter/non-responder strains differed as a result of various mutations found within the surface gene. Thus the presence of mutations in preS2 and HBsAg of the non-responding patients may carry predictive markers for nonresponse but further investigation would be needed to conclusively prove this.

Thesis (D Phil. (Medical Virology))--2008. / Background and Objectives: South Africa is one of the countries highly affected by human immunodeficiency virus (HIV) and hepatitis B virus (HBV) infections. Some drugs (e.g. lamivudine) used as part of combination antiretroviral regimens for HIV treatment have dual activity against HBV and HIV. Despite high infection rate with both viruses, routine screening for HBV before initiation of treatment for HIV is not yet a standard practice. This study undertook to investigate: (1) the burden of HBV co-infection in HIV-positive patients enrolling for highly active antiretroviral therapy (HAART) at Dr George Mukhari hospital, (2) the impact of anti-HBV containing HAART regimens on HBV during the management of HBV/HIV co-infected patients, (3) the co-evolution of HBV and HIV drug-resistant strains, and (4) the correlation of HBV genotypes with response to anti-HBV containing HAART regimens. Study Population and Methods: To investigate the burden of HBV/HIV co-infections, a cohort of 192 HIV patients who were candidates for ARV treatment at Dr George Mukhari hospital were studied by screening for HBV serological markers (HBsAg, anti-HBs and anti- HBc) (Elecsys 2010, Roche Diagnostics) and HBV DNA with an in-house nested PCR assay targeting HBV polymerase gene. Quantitation of HBV DNA positive samples was performed with Roche Cobas Taqman HBV test 48 assay. To investigate the impact of lamivudine-containing HAART regimens on HBV during the management of HBV/HIV co-infected patients, as well as the coevolution of HBV and HIV drug-resistant strains, a total of 78 patients were studied. HBV virological response against lamivudine containing-HAART regimens [1a (lamivudine, stavudine and efaverenz); 1b (lamivudine, stavudine and neviripine)] was measured (Cobas Taqman HBV test 48, Roche diagnostics). HBV direct sequencing targeting HBV polymerase gene was performed on all baseline samples (n=78) and additional samples collected at various time points (n = 45). Direct sequencing was also performed on 30 HIV baseline samples targeting the HIV reverse transcriptase and protease genes (Spectru-Medix SCE 2410 Genetic Analysis System and ABI PRISM® 3100 Genetic Analyzer version 3.7). To explore the genetic diversity of HBV and HIV strains circulating in Pretoria and surrounding areas, as well as the correlation of HBV genotypes with response to lamivudine-containing-HAART regimens in co-infected patients, all baseline and follow-up HBV and HIV sequences were analysed, compared and correlated with treatment. Sequence alignments and phylogenetic studies for both HBV and vi HIV were conducted with MAFFT, Mega 4 and neighbour joining phylogenetic trees generated with the PHYLIP programme. Results: Three significant findings were observed in this study. Firstly, the majority of South African HIV patients enrolling for HAART were exposed to HBV infection and either had acute or chronic HBV infections. A total of 63.0% of patients were found to have one or more HBV markers, with 40.6% having detectable HBV DNA as an indication of replication. The study also detected 22.9% with positive HBsAg, and 23% of 77% HBsAg-negative patients having occult hepatitis B infection. Secondly, HBV/HIV co-infected patients do benefit during the management of HIV infections with lamivudine-containing HAART regimens. A total of 68.4% of patients responded to HAART, with undetectable HBV DNA during 18 to 24 months of follow-up. A total of 91.3% of HIV patients also responded to HAART with an undetectable HIV viral load during 6 to 12 months of follow-up. However, a total of 18% of patients had persistent HBV DNA, yielding various HBV virological responses against lamivudine containing-HAART regimens. This proportion of patients poses a question regarding the management of HBV and HIV coinfections, as guidelines on the use of HAART with anti-HBV activity from developed countries, may not necessarily be followed in developing countries. The results further showed that baseline drug-resistance was more frequent with HIV than HBV in this cohort of patients. The following HIV primary drug resistant mutants were observed: nine major NRT's primary mutants, M41L (1/30), E44A (1/30), V75M (1/30), F77L (1/30), V118I (1/30), M184V (1/30), L210S (1/30), T215Y (1/30) and V90I (1/30), and five major NNRT’s primary mutants were also detected, K103N (3/30), Y318CFSY (1/30), E138Q (1/30), P225H (1/30) and K238T. However, all followup samples had undetectable HIV viral load. In contrast to HIV, only one patient was detected with HBV mutant, M204I, at baseline. The mutant reversed to wild type during 6 months and other follow-up (12, 18 and 24 months). Finally, this study indicated that the HBV genotype A is still the most prevalent genotype circulating in South Africa. Of the 78 HBV sequences, 77 were genotype A and 1 sequence was genotype G. This is the first report from Africa of the detection of HBV genotype G. HIV subtype C remains the predominant prevailing subtype in South Africa. HBV genotype or HIV subtype C was not observed to influence any treatment outcome following treatment with vii lamivudine-containing HAART regimens. The study also indicated that patients on lamivudinecontaining HAART regimens do benefit not only by suppressing HIV and HBV viral load, but also improving immunity (i.e. CD4 cells count increases). Conclusion: Overall, the present study highlights the need for screening HBV before initiation of any HAART containing anti-HBV regimens in HBV/HIV co-infected patients. It necessitates the use of molecular assays for effective laboratory in diagnosis of occult HBV infections in HIVpositive patients, especially in developing countries where these assays are not widely available. While lamivudine-containing HAART regimens do benefit both HBV and HIV patients in co-infected individuals, however, whether HBV virological response is temporary or sustained is unknown at this stage. What is certain is that these patients require an effective monitoring programme as (1) a small percentage experience variable HBV virological responses (partial, reactivation, or no response), and (2) hepatitic flares are likely to develop if HAART is terminated (e.g. by patient), or the current HAART regimen is switched to another regimen without anti-HBV activity. HBV genotype A remains the dominant genotype in South Africa, but novel genotypes can be detected. HIV subtype C was found to be the prevalent subtype. HBV genotype or HIV subtype C were not seen to influence any treatment outcome following treatment with lamivudine-containing HAART regimens. Recommendations: HIV patients should be screened for HBV before initiation of anti-HBV containing HAART regimens. The screening of HBV in HIV patients is also important since some drugs included as part of HAART (e.g. nevirapine) may cause hepatotoxicity and exacerbate HBV infections leading to increased morbidity and mortality due to liver complications. Immunization and immune boosters of HIV patients with low (< 10IU/L) or no immunity against HBV should be done as this could be beneficial, although these patients may not respond optimally, or their immunity may wane faster due to immunocompromised status. Monitoring of both HBV and HIV resistant strains should be conducted for timely detection for the occurrence of multiple resistant mutations, which could limit future therapeutic option for both viruses.

The recombinant Hepatitis B surface antigen vaccine inadequately protects those living with HIV from Hepatitis B virus infection. This study utilized saved serum samples from a retrospective cohort of persons with HIV and documented vaccine-induced HBsAb seroconversion to determine factors associated with persistence of protective levels of HBsAb (≥10mIU/ml). HBsAb levels fell below 10mIU/ml in 27% of the cohort after a median follow-up of 43 months. HIV viral load suppression (<50copies/ml) at the time of vaccination was the major factor associated with persistence of protective levels of HBsAb (OR 3.83, p <0.01). Among individuals who lost protective levels of HBsAb, booster doses of vaccine re-instated the development of protective levels of HBsAb. Delaying or repeating HBV vaccination until after suppression of HIV viral load is achieved should be considered HBV antibody levels should be followed over time and boosters given with loss of protective levels of HBsAb.

The recombinant Hepatitis B surface antigen vaccine inadequately protects those living with HIV from Hepatitis B virus infection. This study utilized saved serum samples from a retrospective cohort of persons with HIV and documented vaccine-induced HBsAb seroconversion to determine factors associated with persistence of protective levels of HBsAb (≥10mIU/ml). HBsAb levels fell below 10mIU/ml in 27% of the cohort after a median follow-up of 43 months. HIV viral load suppression (<50copies/ml) at the time of vaccination was the major factor associated with persistence of protective levels of HBsAb (OR 3.83, p <0.01). Among individuals who lost protective levels of HBsAb, booster doses of vaccine re-instated the development of protective levels of HBsAb. Delaying or repeating HBV vaccination until after suppression of HIV viral load is achieved should be considered HBV antibody levels should be followed over time and boosters given with loss of protective levels of HBsAb.

Objetivo : Determinar los factores de riesgo asociados a la transmisión del virus de la Hepatitis B (VHB) en el Centro Médico Naval durante el período de estudio. Material y métodos : Estudio de casos y controles. Se evaluaron los pacientes hospitalizados en la Sala de Enfermedades Transmisibles con el diagnóstico de Síndrome ictérico mas hipertransaminasemia ( TGO y/o TGP > 500 u/l ). Los factores de riesgo reportados entre los sujetos infectados con el VHB (B+); fueron comparados con los sujetos no infectados (B-), mediante el análisis bivariado y multivariado. Resultados : Un total de 74 sujetos fueron evaluados serológicamente para VHB, de los cuales 37 fueron positivos ( 35 infección aguda y 2 infección no aguda ). Los sujetos B+ fueron en su mayoría de sexo masculino y tuvieron como factor de riesgo mas significativo una hospitalización previa ( OR:13.33 ). Además se describen los cuadros clínicos y exámenes de laboratorio encontrados en ambos grupos. Conclusión : La fuerte asociación encontrada entre hepatitis B y hospitalización previa, sugiere que la transmisión horizontal nosocomial tiene un rol protagónico en la transmisión del VHB en el Centro Médico Naval.

published_or_final_version / Medicine / Master / Doctor of Medicine

No description available.

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.