M.Sc.(Med.), Faculty of Health Sciences, University of the Witwatersrand, 2011 / Hepatitis B virus (HBV) and human immunodeficiency virus (Thakur et al.) are endemic in South Africa. There no data on the HBV genotypes prevailing in HIV-infected South Africans. The aim this study was to determine the HBV genotypes in HIV-infected patients and to identify mutations occurring in the basic core promoter/preccore (BCP/PC) and complete S regions. Twenty six HBV isolates from HBV-HIV co-infected individuals from Helen Joseph urban hospital prior to and at six month after initiation of HAART were analyzed. Three hundred HBV isolates from the rural Shongwe Hospital were recruited prior to treatment. Restriction fragment length polymorphism (RFLP) together with sequencing of the BCP/PC and complete surface region amplicons were employed for genotyping and analysis. There was no significant difference in the HBV genotypes from both cohorts. Subgenotype A1 was the predominant genotype. HBV DNA was detected in 13/26 (50 %) Helen Joseph patients and 72/300 (24%) HBV DNA was detected in patients from Shongwe cohort: 28/300 (9.3%) HBsAg-positive and 44/300 (14.7%) HBsAg-negative. The BCP/PC region of HBV isolates from both cohorts showed mutations that could account for the HBeAg negativity, although in the case of the Helen Joseph cohort the HBeAg status was unknown because of depletion of serum. The HBeAg negativity in 44/49 Shongwe patients (89,7%) could be accounted for by the following mutations: 1) the basic core promoter mutations T1753C A1762T G1764A, which down regulate transcription of precore mRNA; 2) the Kozak sequence mutants that affect HBeAg translation, 3) the G1862T mutation, which interferes with post-translational modification of the HBeAg-precursor, and 4) the classical G1896A stop codon mutation with C1858T. The G1862T mutation occurred in HBV from 24.1% HBsAg-positive Shongwe patients but in none of the HBsAg-negative patients (p<0.05). PreS deletion mutants were found in isolates from both cohorts. These have previously been described in hepatocellular carcinoma patients. The Helen Joseph HBV isolates had the “a” determinant and immune/vaccine escape mutants. In addition to these, Shongwe isolates had HBV reactivation markers mutations V168A + S174N in 23.8% of the HBsAg-negative and in none of the HBsAg-positive infections. Drug resistant mutations were found in three Shongwe HBV isolates from ART naïve individuals and in none Helen Joseph HBV isolates. In conclusion, South African HIV-infected individuals were predominantly infected with subgenotype A1 of HBV. Mutations in the BCP and precore region of HBV isolates could account for the HBeAg negativity in the majority of patients. A number of HBV isolates displayed both immune escape and drug resistance mutations that were responsible of the HBsAg-negativity in patients from which they were isolated.

Members of the family Hepadnaviridae have been detected in both avian and mammalian species. They have a very limited host range, and among the nonhuman primates, have been found to occur naturally in chimpanzees, gorillas, gibbons, orang-utans and woolly monkeys. The human hepatitis B virus (HBV) has been shown to infect chimpanzees, Barbary macaques and tree shrews. During the course of a previous study, to determine the susceptibility of baboons (Papio ursinus orientalis) to HBV infection, HBV DNA was detected in the serum of 2 baboons prior to their inoculation with HBV-positive human serum, raising the possibility that baboons are naturally infected with a hepadnavirus. Therefore the aim of this study was to determine the prevalence of HBV in wildcaught baboons and to molecularly and functionally characterise the virus isolated from these baboons. DNA was extracted from the sera of wild-caught baboons and four separate regions of the HBV genome amplified by nested polymerase chain reaction (PCR). Samples were only considered to be positive for HBV if at least three of these regions amplified. DNA was extracted from the liver tissue of one of the HBV DNA-positive baboons using a proteinase K digestion followed by a phenolchloroform extraction and ethanol precipitation. From this extract, the complete HBV genome was amplified by nested PCR of eight overlapping subgenomic fragments, and sequenced. This sequence was analysed phylogenetically using both the PHYLIP and Simmonic software packages. A selective real time PCR using SYBR®-green detection was used to detect covalently closed circular (ccc) DNA. RNA was extracted from the baboon liver tissue using a guanidinium-acidphenol extraction method, reverse transcribed and portions of the HBV genome amplified by nested PCR. Transmissibility of the virus was tested by injecting four experimentally naïve baboons individually with serum from four HBV DNApositive baboons and followed for 26 weeks. HBV was detected in the serum of 5/69 (7,2%) wild-caught baboons by Southern hybridization and in 11/49 (22,4%) adult and 4/20 (20,0%) juvenile wild caught baboons. This gave an overall prevalence of 21,7% in the baboon population surveyed. Serologically, the baboon sera were negative for all markers of HBV infection and alanine aminotransferse (ALT) levels were normal. In the one baboon liver tissue available, HBcAg was detected by immunohistochemical staining in some of the hepatocyte nuclei, but HBsAg was not detected. Phylogenetic analysis of the complete genome of the HBV isolate found it to cluster with subgenotype A2, a surprising result considering that subgenotype A1 predominates in South Africa. However, unlike other subgenotype A2 isolates, the basic core promoter had the G1809T / C1812T double mutation characteristic of subgenotypes A1 and A3 and the precore region had the G1888A mutation unique to subgenotype A1. These mutations in the basic core promoter and precore regions have previously been shown to reduce the expression of the precore and core proteins. Four additional mutations in the polymerase, surface, X and core open reading frames (ORFs) further differentiated the baboon HBV strain form the majority of previously sequenced subgenotype A2 isolates. cccDNA was detected at low levels in the baboon liver tissue. Regions of the precore/core and surface ORFs were amplified off reverse transcribed cDNA. These results demonstrate HBV replication in the baboon liver. Transmission of the virus was shown by the detection of HBV DNA in the sera of the four inoculated baboons at various times throughout the 26 week follow-up period. These baboons also showed transient seroconversion for HBsAg and HBeAg during this period with intermittent fluctuations in ALT levels. Moreover, using DNA extracted from liver tissue obtained at necropsy from one of the injected baboons, the sequence of the HBV surface gene amplified was found to be identical to the sequence of the isolate from inoculum. The finding of subgenotype A2 in the baboon is paradoxical because subgenotypes A1 and A3 as well as genotypes D and E predominate in Africa. The possibility exists that subgenotype A2 is an older strain that has been overtaken by these other strains. There is however a scarcity of subgenotype A2 sequencing data from Africa and a higher circulation of this subgenotype could be uncovered with more extensive molecular epidemiological studies in more remote areas. Alternatively, a recent discovery of alternative compartmentalization of subgenotype A2 infections in the peripheral blood lymphocyte population of individuals from India, where subgenotype A1 also predominates, could explain the lack of detection of this subgenotype in Africa. Occult hepatitis B infection is defined as the presence of HBV DNA in the liver (with detectable or undetectable HBV DNA in the serum) of individuals testing negative for HBsAg by currently available assays. The detection of HBV DNA in the baboon liver and serum in the absence of serological markers therefore classifies this infection as occult. To our knowledge, this is the first study to demonstrate a naturally occurring occult HBV infection in non-human primates.

Hepatitis B virus (HBV) has been found to be highly endemic in Africa and south east Asia. In southern Africa, subgenotype A1 and genotype D prevail while in south east Asia genotype B and C predominate. Infection with HBV can lead to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma (HCC). It has been shown that viral factors as well as a number of host and environmental factors can influence the course of HBV infection. Development and progression of various liver diseases are associated with either an increase or decrease in hepatocyte apoptosis. Dysregulated apoptosis itself may be a fundamental feature of most acute and chronic human liver diseases. The purpose of this study was to characterise the subgenotype A1 and genotype D HBV infection, prevailing in South Africa. To control for the influence of host factors on HBV infection as well as to avoid the use of in vitro cell lines, such as Huh-7, that have defective apoptotic pathways, the in vivo urokinase plasminogen activator severe combined immunodeficient (uPA-SCID) transgenic mouse model was utilised. The HBV infection of the transgenic mice infected with HBV positive sera containing either subgenotype A1 wildtype, subgenotype A1 with the G1862T mutation, subgenotype A2 or genotype D, was compared. For the first time, we were able to demonstrate the successful infection of the uPA-SCID transgenic mouse model with subgenotype A1 of HBV. The successful establishment of the in vivo HBV infection with different genotypes or subgenotypes in the uPA-SCID transgenic mice was demonstrated by the increase of HBV DNA levels, the presence of cccDNA and HBV transcripts as well as the detection of the core and/or surface HBV antigens in the liver tissue of the chimeric mice. Differences between the HBV infections with the various genotype/subgenotypes were observed. Subgenotype A1 with the G1862T mutation showed the earliest detection and therefore highest levels of cccDNA as well as the highest HBV DNA levels when compared to the other strains. The highest HBV DNA levels were recorded for the subgenotype A1 G1862T infected transgenic mouse followed by genotype D, subgenotype A2 and the lowest levels observed in the subgenotype A1 wild-type infected transgenic mouse. HBsAg was also only detected in the livers of mice infected with subgenotype A1 with the G1862T mutation. HBcAg staining in the chimeric liver was positive when the mice were infected with genotype D, which concurs with previous observations that genotype D is characterised by high HBcAg expression. Subgenotype A1 with the 1862 mutant showed the highest levels of apoptosis as a result of the abnormal precore precursor protein accumulation shown to be associated with this 1862 missense mutation. Thus different genotypes and subgenotypes as well as variations within genotypes can influence HBV infection. Moreover, the results of these experiments in the immunocompromised chimeric mice, grafted with liver cells from a single donor, suggests that even when host and environmental risk factors are controlled for, the subgenotype or genotype can influence the course of infection. The limitations of the uPA-SCID transgenic mouse model include the lack of an immune system and the short life-span of the animal; therefore a population based study was carried out to investigate the influence of host factors on HBV infection in various disease groups. The study cohort comprised 635 serum samples from South Africa, China and Japan. Of these samples, 564 were HBsAg-positive and the remaining 71 HBsAg-negative, HBV DNA negative controls. The study cohort included asymptomatic carriers; chronically infected HBV patients as well as patients with HBV associated HCC. Possible associations were determined between HBV genotype, HBV viral load, apoptosis levels, disease group and the age and gender of the patient where available. Apoptosis levels were quantified by the measurement of cleaved cytokeratin 18 (M30) in serum. Patients infected with genotype C or subgenotype A1 were shown to possess a higher odds ratios of developing HCC compared to subgenotype B2 or genotype D, respectively. Significantly higher HBV viral loads were observed in genotype C compared to subgenotype B2. Among the Asian cohort, it was also shown that the male gender was positively associated with high viral loads in HCC patients. Moreover, a positive association between higher HBV viral load levels and HCC in the South African cohort was observed. Male gender, older age, HBV viral load, subgenotype A1 and the presence of the G1862T mutation were shown to be positively and significantly associated with higher levels of apoptosis. In this study it was discovered that the levels of cleaved cytokeratin 18 could potentially be used as a biomarker for the severity of HBV infection because a significant difference was observed with the apoptosis levels between the asymptomatic and HCC patient disease groups. We conclude that even when the influence of host and environmental factors is controlled for, as is the case in the chimeric mouse model, the HBV genotype can affect the progression of infection. Moreover, it was shown in the population based study that the effect of HBV genotype on the outcome of HBV infection can be influenced by host factors. The subgenotype A1 G1862T mutation was shown in both studies to affect both HBV infection and apoptosis. This suggests that HBV variants should be investigated to ascertain their potential impact on the course of HBV infection as it may differ from the wild-type. Apoptosis was shown to be associated with HBV infection in both studies and could possibly be an ideal marker of the progression of HBV infection. These findings are important in helping us to understand factors influencing the course of HBV infection. We have therefore shown in both the studies that differences do exist between the South African subgenotype A1 and genotype D, and that these differences should be taken into consideration for the future evaluation of HBV infection and treatment of South African HBV infected patients. Moreover, cleaved cytokeratin 18 may provide an ideal surrogate marker for HBV disease progression and monitoring.

by Chan Lik-yuen, Henry. / Thesis (M.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 192-217). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

Worldwide there are 350 million people with chronic hepatitis B infection and globally it causes up to half of the liver cancer deaths and one third of deaths from cirrhosis. Only a fraction of sufferers will develop these complications. Various studies have implicated socio-demographic, biochemical and viral factors in disease progression but research has been limited to local populations in endemic countries. Our aim was to study the prevalence and factors associated with advanced disease of hepatitis B infection in immigrants living in East London. I completed a retrospective analysis of notes and electronic health records of 1209 immigrant patients attending hospitals in East London, 217 of whom were from Bangladesh and Pakistan. Screening of volunteers attending local mosques using oral mucosal transudate swabs and national statistics data allowed us to calculate prevalence rates in these populations. Those 13 patients from Bangladesh and Pakistan admitted over 30 months with decompensated disease were men aged > 40. Age, sex, ALT, smoking, alcohol and diabetes were significant predictors for cirrhosis and decompensated disease but not viral markers. Similar analyses were performed for other ethnicities with similar outcomes. The scale of under diagnosis of hepatitis B for all ethnicities was estimated and the reasons explored. This work has scrutinised the epidemiology of chronic hepatitis B in East London and the difficulties encountered exploring it. We provide differing results to published studies and suggestions for how this domain can be examined further.

Introduction and aims: In the United Kingdom hepatitis B virus (HBV) and hepatitis C virus (HCV) disproportionately affect migrants and people who inject drugs (PWID). Ascertainment rates of HBV and HCV are 10-40% and screening is recommended in at risk groups. Treatment uptake for HCV in PWID is low at 2-18%, and the most effective way to increase uptake is not known. This research aims to evaluate methods to address the low ascertainment and treatment rates of HBV and HCV in these populations. Methods: A pilot observational cohort study of screening for chronic viral hepatitis in primary care. A retrospective observational cohort study into outcomes of HCV treatment in PWID. A prospective cluster randomised trial of nurse versus doctor initiated treatment for HCV in PWID and a qualitative analysis exploring the engagement with treatment for HCV of PWID. Results: Direct testing results in a greater uptake of screening than opportunistic testing in migrants in primary care (21% versus 1.9%, p = < 0.0001). PWID have SVR rates of 55%, re-infection rates of 2.4 per 100 person years, and crack cocaine use reduces over treatment (90% to 49%, p= < 0.0001). Nurse initiation of treatment does not result in a higher uptake of therapy (9.6 % versus 7.8%, p=0.53). Treatment engagement themes included the normalisation and stigmatisation of HCV and the perception of HCV treatment as a transformative process. Discussion: Direct testing for HBV and HCV appears to result in a greater uptake of testing in migrants in primary care and should be investigated in a randomised controlled trial. HCV treatment in PWID is safe and effective, and illicit drug use may reduce over treatment. Further service development is unlikely to result in a greater uptake of antiviral therapy for HCV in PWID and other options should be explored to improve treatment uptake.

Publicación a texto completo no autorizada por el autor / Refiere que la hepatitis inducida por drogas antituberculosis (HID) es una reacción adversa frecuente de los fármacos empleados en el tratamiento de la tuberculosis (RAFA). La ausencia de un reto con drogas antituberculosis establecido con un régimen adaptado a nuestra realidad, que incluya 4 drogas, y que no sea muy prolongado para evitar la transmisibilidad de la tuberculosis, hace necesaria la investigación de regímenes cortos, con alto valor predictivo, y con margen de seguridad aceptable, y que ya se han venido efectuando. Se realizó un estudio descriptivo retrospectivo longitudinal de todos los casos presentados en el Hospital Rebagliati entre 2000 y el 2011 a quienes fueron retados luego de haber presentado hepatitis inducida por drogas antituberculosis, una vez remitida. Se identificaron 30 casos de HID secundaria a esquema 1, en 17 hombres y 13 mujeres, entre las edades de 14 a 91 años. En el 60% de casos solo con compromiso hepático y en 40% con compromiso sistémico. Se aplicaron varias modalidades de retos, encontrándose una mayor proporción de identificación de droga injuriante, así como una subsecuente menor recurrencia de la RAFA cuando se retó con las 4 drogas de primera línea. Otros factores relacionados a recurrencia fueron alteraciones clínicas y laboratoriales desestimadas durante los retos; y perfil hepático anormal al final de los retos. Hubo 2 casos mortales que estuvieron relacionados a edad avanzada y desnutrición. / Trabajo académico

Thesis (MPH)--University of Limpopo, 2009. / BACKGROUND AND AIM: Hepatitis B virus (HBV) is the major cause of hepatitis in South Africa (SA), with an estimated 4 million carriers. It is transmitted by infected blood and other body fluids, placing health care workers (HCWs) at high risk of infection. The SA Department of Health strongly recommends that all HCWs be vaccinated against HBV, but studies have shown that uptake of the vaccine is sub-optimal. This study aimed to estimate HB vaccination coverage levels among nurses, and describe the demographics and characteristics of the HB vaccination policies associated with different levels of coverage, at private and public hospitals in Tshwane. METHODS: This was a questionnaire-based cross-sectional study on 300 randomly selected nurses and 12 chief infection control officers (CICOs) from 13 hospitals (6 public and 7 private) in Tshwane performing high risk procedures. CICOs were asked questions about HB vaccination policies and coverage, while nurses were asked about demographics, HB vaccination status, and the HB vaccination policies of their institutions. RESULTS: The response rate was 84.3% (253/300) for nurses, and 75% (9/12) for CICOs. Of the nurses, 68.0% (172/253) were vaccinated, and logistic regression analysis found that those statistically significantly most likely to be vaccinated were: 30 years and younger (odds ratio [OR]=2.9; 95% CI: 1.11–7.59); employed in private hospitals (OR=3.0; 95% CI: 1.24–7.32); and graduated after 1990 (OR=2.6; 95% CI: 1.10–6.19). Also, logistic regression analysis found two statistically significant policy-related predictor for vaccination uptake, which was the presence of HB vaccination program (OR=4.6; 95% CI: 2.11-10.06); and compulsory HB vaccination (OR=2.8; 95% CI: 1.37-5.70. CONCLUSION: There is a need for a national policy on HB vaccination of HCWs which should include compulsory vaccination, to increase the vaccination coverage level amongst nurses.

Thesis (MSc. (Medical Virology))-- University of Limpopo, 2011. / Introduction: Sub-Saharan Africa is a region with hepatitis B virus (HBV) hyperendemicity with more than 8% HBsAg prevalence. An estimate of two billion people has been reported to carry HBV markers. HBV was associated with about 25% of annual deaths in Africa. HBV possesses a DNA polymerase which lacks proofreading mechanism. This results in highly variability and genetic diversity which poses a challenge for the diagnosis and therapeutic management of HBV infection. High mutation rate of HBV also has great implications on the development of drug resistant mutations. Moreover, HBV diversity represents a challenge for the sensitivity of immunological and molecular diagnostic assays. A number of studies on HBV full length genome have been conducted particularly in developed countries. Limited studies are available in Africa and South Africa. In South Africa, few studies have been done analysing the complete genome of HBV isolates from patients with asymptomatic carriers and fulminant hepatitis B (Owideru et ai, 2001 a; Owideru et ai, 2001 b; Kimbi et ai, 2004; Kramvis et ai, 2002).This study was aimed at characterising the full-length genome of HBV isolates at Dr George Mukhari Hospital, Pretoria, South Africa, with a view of developing a PCR-based technology for amplification and characterisation of HBV strains with different serological profiles. The technology, if successfully developed, will contribute in understanding the molecular mechanisms resulting in various HBV variants or isolates. Methods: The study design was exploratory. Four stored serum samples collected from HBV infected patients at Dr George Mukhari hospital, Pretoria, were used to develop the molecular technology and test the hypothesis. HBV serology was previously performed targeting 5 HBV serological markers; HBsAg, anti-HBs, anti-HBc, HBeAg and anti-HBe using Elecsys version; HBV DNA quantification was done using Cobas Amplicor HBV DNA monitor assay, HBV DNA was extracted and subjected to nested PCR assay targeting HBV full length genome as two overlapping fragments: fragment A (1670 bp) and fragment B (1868 bp). The generated PCR products for both fragments were cloned into the pGEM T easy vector and 2 clones were selected from each sample. The plasm ids were purified using Invisorb@ Spin Plasmid Mini Two and the clones were recovered by PCR assay. The sample PCR products and the clone PCR products were purified and sequenced using SpectruMedix SCE2410 genetic analysis system. HBV genotyping was performed using the NCBI web-based genotyping tool. Phylogenetic analysis was done using MEGA 4 software to confirm HBV genotypes. Results: Serology results were as follows: All samples were HBsAg positive, Anti-HBs negative, anti-HBc positive and anti-HBe negative. Sample B1121 and sample 6 were HBeAg positive while samples B452 and 5 were HBeAg negative. A total of 12 PCR products were sequenced (4 study samples and 8 clones [2 clones each sample]). In total, 7 HBV full length genome sequences were deduced from this study, with 3 sequences belonging to genotype A, 2 to genotype C and 2 to genotype D. 3 HBV genotypes were detected from this study; genotype A, C and D with subgenotype A2, C1 and D1 respectively. Mutations were observed throughout the genome. In the pre-S/S open reading frame (ORF), the most significant findings were the detection of mutations within the "a" determinant site and major hydrophilic region (MHR). These mutations included Y161F,E164G observed in sample B1121 and B1121C1 belonging to subtype A1; 2 amino acid insertion at aa 161-162 in sample 5 belonging to subtype C1. Drug resistance associated mutations were identified in the polymerase gene, these included M204T and L217R which are associated with adefovir resistance, M204T also resulted in a change from tryptophan (W) to arginine (R) at aa 196 on the overlapping surface gene on sample B452 C1. Basal core promoter (BCP) and pre core/core mutations were detected in study isolates; specifically the BCP double mutation (1762/1764) was seen in 8 isolates which belonged to subtype C1 (5) and D1 (3) and the pre-core stop codon mutations (G1896A) in 4 isolates. (2 belonging to subtype C1 and the other 2 to D1). Other changes observed included a 48 nucleotides deletion in the pre-core gene, 6 nucleotides insertion in the HBx gene of all subtype D1 isolates and a 3 nucleotides deletion in subtype C1 clone. Conclusion: This study successfully optimised a PCR-based technology for the amplification and characterisation of HBV full length genome. 3 HBV genotypes were detected with subtypes A2, C1 and D1. However, the detected subtypes are rarely detected in South Africa. The detection of subtype A2 may confirm its Southern African origin. Drug resistance associated mutations were observed in this study. These included the adefovir resistance mutation which the current study confirmed it is a naturally occurring mutation as it was detected in adefovir therapy na'ive patient. The BCP and pre-core/core mutations were detected in genotype C and D isolates; however, their association with serological profile and clinical outcomes could not be deduced. Unique or novel mutations were seen in the study isolates, these included 48 nucleotides deletion in the pre core gene, 3 amino acids insertion in the RNase H and 8 amino acids deletion in the RT domain of polymerase gene. To our knowledge, these mutations have not been identified or reported in the literature. The detection of 6 nucleotide insertion in the HBx gene was reported for the first time in South African isolates. Further analysis is required to ascertain the biological significance of the unique mutations detected in this study.

Sub-Saharan Africa has a high prevalence of hepatitis B virus (HBV) infections. Health care workers (HCWs) are at high risk of contracting HBV infection through their occupation. Vaccination of HCWs against HBV is standard practice in many countries, but is often not implemented in resource-poor settings. We aimed with this cross-sectional study to determine HBV prevalence, HCW vaccination status, and the risk factors for HCWs contracting HBV infection in Tanzania. We enrolled 600 HCWs from a tertiary Tanzanian hospital. Their demographics, medical histories, HBV vaccination details and risk factors for contracting blood-borne infections were collected using a standardized questionnaire. Serum samples were tested for HBV and hepatitis C virus (HCV) markers by ELISA techniques, PCR and an anti-HBs rapid test. HCWs were divided in two subgroups: those at risk of contracting HBV (rHCW 79.2 %) via exposure to potentially infectious materials, and those considered not at risk of contracting HBV (nrHCW, 20.8 %). The overall prevalence of chronic HBV infection (HBsAg+, anti-HBc+, anti-HBs-) was 7.0 % (42/598). Chronic HBV infection was found in 7.4 % of rHCW versus 5.6 % of nrHCW (p-value = 0.484). HCWs susceptible to HBV (HBsAg-, anti-HBc-, anti-HBs-) comprised 31.3 %. HBV immunity achieved either by healed HBV infection (HBsAg-, anti-HBc+, anti-HBs+) or by vaccination (HBsAg-, anti-HBc-, anti-HBs+) comprised 36.5 % and 20.2 %, respectively. 4.8 % of participants had indeterminate results (HBsAg-, anti-HBc+, anti-HBc-IgM-, anti-HBs-). Only 77.1 % of HCWs who received a full vaccination course had an anti-HBs titer >10 ml/U. An anti-HBs point-of-care test was 80.7 % sensitive and 96.9 % specific. There was a significantly higher risk for contracting HBV (anti-HBc+) among those HCW at occupational risk (rHCW) of older age (odds ratios (OR) in rHCW 3.297, p < 0.0001 vs. nrHCW 1.385, p = 0.606) and among those HCW being employed more than 11 years (OR 2.51, p < 0.0001***). HCV prevalence was low (HCV antibodies 1.2 % and HCV-RNA 0.3 %). Chronic HBV infection is common among Tanzanian HCWs. One third of HCWs were susceptible to HBV infection, highlighting the need for vaccination. Due to high prevalence of naturally acquired immunity against HBV pre-testing might be a useful tool to identify susceptible individuals. / Die Studie konnte in einem Krankenhaus der Maximalversorgung im Norden Tansanias eine hohe Prävalenz chronischer Hepatitis B-Infektionen beim Gesundheitspersonal zeigen. Weiterhin hatten die Teilnehmer ein hohes Risiko, eine HBV-Infektion im Laufe ihres Berufslebens zu erwerben. Bezüglich der Hepatitis C-Infektion zeigte sich insgesamt eine sehr niedrige Prävalenz. Ein besonders hohes Risiko, mit Hepatitis B infiziert zu werden, hatte Personal mit direktem Kontakt zu Blut oder Nadelmaterial. Ein Drittel des Krankenhauspersonals wies keine Immunität gegen Hepatitis B auf und war somit weiterhin einem Infektionsrisiko ausgesetzt. Etwas mehr als ein Drittel des Kollektivs wies die Antigen-/Antikörperkonstellation einer ausgeheilten Infektion auf. Der Infektionszeitpunkt ist aufgrund der häufig inapparenten klinischen Verläufe retrospektiv nicht zu eruieren. Ein weiterer Teil konnte mittels Immunisierung durch eine bereits im Vorfeld durch Hilfsgelder finanzierte Impfaktion eine Immunität erwerben. Der Impferfolg wurde nach dieser Impfaktion jedoch nicht serologisch verifiziert. Bei 40 Personen, die angaben an der Impfaktion teilgenommen zu haben, konnten keinerlei Antikörper nachgewiesen werden. Retrospektiv zeigte die Impfaktion mit 76% eine niedrige Erfolgsrate, was unter anderem auf einen hohen Teil an bereits HBV-Infizieren Teilnehmer zurückzuführen ist, bei denen eine Impfung nutzlos ist.