• BCP
• C gene
• Hepatitis B virus
• P gene
• PC
• S gene

• Humans
• Hepatitis B virus/genetics
• Hepatitis B virus/classification
• Hepatitis B virus/isolation & purification
• Blood Donors
• Genotype
• Hepatitis B/virology
• Hepatitis B/epidemiology
• Male
• Genetic Variation
• Female
• Adult
• Middle Aged
• Hepatitis B Surface Antigens/genetics
• Hepatitis B Surface Antigens/blood
• Timor-Leste/epidemiology
• Mutation
• Young Adult
• DNA, Viral/genetics
• Phylogeny

• Genotype C
• Hepatitis B virus (HBV)
• Sub-genotype C1
• r269L Type
• rt269I type

• Hepatitis B virus/genetics
• Hepatitis B virus/classification
• Humans
• Promoter Regions, Genetic/genetics
• Phylogeography
• Genotype
• Mutation
• Phylogeny
• Hepatitis B, Chronic/virology
• Hepatitis B, Chronic/epidemiology
• Genome, Viral
• Male
• Hepatitis B/virology
• Hepatitis B/epidemiology

Immunization programmes against hepatitis-B are being carried out since more than three decades but still HBV is a major public health problem. Hepatitis B virus (HBV) genome consists of circular and partial double stranded DNA. Due to partial double stranded DNA, it uses an RNA intermediate during replication. This replicative strategy of HBV and lack of polymerase proofreading activity give rise to error occurrences comparable to retroviruses. The low fidelity of polymerase, overlapping reading frames and high replication rate produces many non-identical variants at every cycle of replication. Therefore, HBV spreads with mutations and variations. The mutations have been reported both in non-structural as well as structural genes of HBV genome. Recent advances in molecular biology have made easier to analyse these mutations. Hepatitis B antiviral therapy and immunization are all influenced by genetic variability. The analysis and understanding of these mutations are important for therapy against hepatitis B and updating of diagnostic tools. The present review discusses about mutations occurring in whole HBV genome. The mutation occurring both in structural and non-structural genes and non-coding regions have been described in details. It is much more informative because most of literature available, covers only individual gene or DNA regions of HBV.

• HBV variants
• Hepatitis B virus
• liver disease
• mutation

• Egypt
• HBeAg
• Hepatitis B
• fibrosis

• Adult
• Aged
• Alanine Transaminase/blood
• DNA, Viral/blood
• Egypt/epidemiology
• Female
• Hepatitis B e Antigens/blood
• Hepatitis B virus/genetics
• Hepatitis B virus/isolation & purification
• Hepatitis B, Chronic/blood
• Hepatitis B, Chronic/epidemiology
• Hepatitis B, Chronic/pathology
• Humans
• Liver/pathology
• Male
• Middle Aged

• Indonesia
• genotype
• hepatitis B virus
• liver disease
• mutation

Hepatitis B virus (HBV) replicates non-cytopathically in the hepatocytes and HBV-related diseases are caused by immune-mediated inflammatory events. This study aimed to identify the relationship between clinical-virological characteristics and immunity in untreated chronic hepatitis B (CHB) patients.

A total of 209 CHB patients were categorized into immune tolerant (IT, n = 17), inactive carrier (IC, n = 20), immune active (IA, n = 120), and gray zone (GZ, n = 72) phases. The quantitative hepatitis B surface antigen (qHBsAg), hepatitis B e antigen (HBeAg), anti-HBeAg (HBeAb), HBV genotype, viral mutant and frequencies of interleukin (IL)-4, IL-17, IL-10 and interferon-gamma (IFN-γ) produced by CD4⁺ and CD8⁺ T cells were tested. We also correlated these cytokines with clinical-virological characteristics using a linear regression model.

CD8⁺ T cells frequency were significantly decreased in IT patients. Levels of CD4⁺ T cells IL-4⁺ or IL-10⁺ were strongly negatively associated with qHBsAg titers. The frequency of IFN-γ produced by CD4⁺ and CD8⁺ T cells showed significant positive association with age and alanine aminotransferase (ALT) level, while that had negative association with qHBsAg titers. Additionally, the ratios of mutations in the HBV precore (PC) stop codon and basal core promoter (BCP) and the combined mutations were 32.5, 27.2, and 11.3%, respectively. The frequency of CD4⁺ T cells IL-17⁺ was higher in patients with a PC mutation than that in patients carrying a wild-type sequence. Finally, little associations among T cell derived IL-4, IL-10, IL-17, and IFN-γ was observed in the current untreated CHB cohort.

Several components of the immune system were correlated with HBV factors that influence an inflammatory process during CHB. Of particular relevance are the significant associations of between CD4⁺ T cells IL-4⁺ and qHBsAg level, and between CD4⁺ T cells IL-17⁺ and the presence of a mutation in PC.

• Chronic hepatitis B (CHB)
• Cytokines
• Linear regression analysis

Viral biomarkers are important tools for monitoring chronic hepatitis B virus (HBV) hepatitis B early antigen (HBeAg) negative infection, both in its natural course as well as during and after treatment. The biomarkers consist of antibodies against viral epitopes, viral proteins, and molecular surrogate markers of the quantity and transcriptional activity of the stable episomal HBV covalently closed circular DNA (cccDNA) which is located in the nuclei of the infected hepatocytes. HBV deoxyribonucleic acid (DNA) or else viral load measurement in plasma or serum is a marker of HBV replication of major clinical importance. HBV DNA is used for staging and treatment monitoring as described in international scientific guidelines. Quantification of HBV antigens, mainly hepatitis B surface antigen (HBsAg) as well as Hepatitis B core related antigen (HBcrAg), play an important yet secondary role, especially in cases of low or undetectable HBV DNA and has been evaluated for the classification of the inactive carrier state, as a predictor of subsequent HBsAg clearance, treatment outcome, and development of hepatocellular carcinoma (HCC). The measurement of the replicative intermediate HBV RNA in serum is currently evaluated and may also prove to be a significant biomarker particularly in patients treated with nucleot(s)ide analogs. This review focuses on the viral biomarkers mentioned above and their role in HBV, HBeAg negative, infection.

• HBV
• HBV DNA
• HBV RNA
• HBcrAg
• HBsAg
• anti-HBe
• biomarker

Drug users act as reservoirs and transmission channels for hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections to the general population worldwide. Periodic epidemiological studies to monitor the prevalence and genetic diversity of these infections to inform on interventions are limited.

The objective of this study was to determine the predictors of HIV infection and genetic diversity of HBV and HCV among drug users in Kenya.

A cross-sectional study on previous drug use history among drug users was conducted in three Kenyan cities using a respondent-driven sampling method between January 2011 and September 2012. Blood samples were collected and analysed for the presence of HBV, HCV and HIV serological markers and to determine the genotypes of HBV and HCV.

The overall prevalence of HBV, HCV and HIV among drug users was 4.3%, 6.5% and 11.1%, respectively, with evidence of HBV/HIV, HCV/HIV and HBV/HCV/HIV co-infections. The HBV circulating genotypes were A1 (69%) and D6 (19%), whereas HCV genotypes were 1a (72%) and 4a (22%). Injection drug use was a significant predictor of HIV/HCV infections. Younger age (30 years; aOR (adjusted odds ratio) = 0.50, 95% CI (confidence interval): 0.33–0.76; p < 0.001) and early sexual debut (aOR = 0.54, 95% CI: 0.40–0.82; p < 0.05) were negatively associated with detection of any of the three infections. Injecting drug use was positively associated with HCV infection (aOR = 5.37, 95% CI: 2.61–11.06; p < 0.001).

This high level of genetic diversity exhibited by HBV and HCV isolates requires urgent implementation of harm reduction strategies and continuous monitoring for effective management of the patients.

Hepatitis B virus (HBV) infection is a common problem in the world, especially in China. More than 60–80% of hepatocellular carcinoma (HCC) cases can be attributed to HBV infection in high HBV prevalent regions. Although traditional Sanger sequencing has been extensively used to investigate HBV sequences, NGS is becoming more commonly used. Further, it is unknown whether word pattern frequencies of HBV reads by Next Generation Sequencing (NGS) can be used to investigate HBV genotypes and predict HCC status. In this study, we used NGS to sequence the pre-S region of the HBV sequence of 94 HCC patients and 45 chronic HBV (CHB) infected individuals. Word pattern frequencies among the sequence data of all individuals were calculated and compared using the Manhattan distance. The individuals were grouped using principal coordinate analysis (PCoA) and hierarchical clustering. Word pattern frequencies were also used to build prediction models for HCC status using both K-nearest neighbors (KNN) and support vector machine (SVM). We showed the extremely high power of analyzing HBV sequences using word patterns. Our key findings include that the first principal coordinate of the PCoA analysis was highly associated with the fraction of genotype B (or C) sequences and the second principal coordinate was significantly associated with the probability of having HCC. Hierarchical clustering first groups the individuals according to their major genotypes followed by their HCC status. Using cross-validation, high area under the receiver operational characteristic curve (AUC) of around 0.88 for KNN and 0.92 for SVM were obtained. In the independent data set of 46 HCC patients and 31 CHB individuals, a good AUC score of 0.77 was obtained using SVM. It was further shown that 3000 reads for each individual can yield stable prediction results for SVM. Thus, another key finding is that word patterns can be used to predict HCC status with high accuracy. Therefore, our study shows clearly that word pattern frequencies of HBV sequences contain much information about the composition of different HBV genotypes and the HCC status of an individual.

HBV infection can lead to many liver complications including hepatocellular carcinoma (HCC), one of the most common liver cancers in China. High-throughput sequencing technologies have recently been used to study the genotype sequence compositions of HBV infected individuals and to distinguish chronic HBV (CHB) infection from HCC. We used NGS to sequence the pre-S region of a large number of CHB and HCC individuals and designed novel word pattern based approaches to analyze the data. We have several surprising key findings. First, most HBV infected individuals contained mixtures of genotypes B and C sequences. Second, multi-dimensional scaling (MDS) analysis of the data showed that the first principal coordinate was closely associated with the fraction of genotype B (or C) sequences and the second principal coordinate was highly associated with the probability of HCC. Third, we also designed K-nearest neighbors (KNN) and support vector machine (SVM) based classifiers for CHB and HCC with high prediction accuracy. The results were validated in an independent data set.

• HBV genotyping
• Hepatitis B virus
• Phylogenetic analysis
• RLFP

• hepatitis B
• nucleos(t)ide analogs
• outcome
• relapse/recurrence
• safety

Mutation of the HBV precore gene prevents the production of HBeAg, which is an important target for immune responses. Distribution of this mutation varies along with frequency of HBV genotypes in accordance with geographic and ethnic variations. The general objective of this study was to evaluate the prevalence and characteristics of precore mutation in Iran and its correlation with genotypes of hepatitis B.

In this cross-sectional study, viral DNA of 182 Iranian hepatitis B surface antigen positive patients who were admitted to Bandar Abbas Blood Transfusion Organization in 2012 and 2013 was retrieved from their serum samples. HBeAg, anti-HBe, and anti-HBc IgM diagnostic tests were performed using ELISA kits. Precore and Pre-S regions were amplified using specific primers and PCR thereafter to determine the genotypes; precore mutation, PCR, and restriction fragment length polymorphism (RFLP) methods also were applied. SPSS version 12 was used for data analysis by Mann–Whitney U test, Fisher’s exact probability test, and t-test.

A total of 62 patients (34.1%) had precore mutation (A1896G), and genotype D was the predominant genotype in these patients, which was followed by an unknown genotype that was suspected for genotype B. Interestingly, the relationships between precore mutation and HBeAg (p=0.037) and genotype D (p=0.005) were significant; however, no correlation was observed between this mutation and acute or chronic hepatitis and sex of patients.

This study found high prevalence of precore mutations in southern Iran, which was significantly associated with HBeAg and genotype D.

• Genotypes
• Hepatitis B
• Precore mutants
• RFLP

Knowledge of hepatitis B virus (HBV) genotype is an important predictive variable which might have an impact in management and treatment of patients with chronic hepatitis B infection. In Ghana very little information is available on hepatitis B genotypes. This study was conducted to determine the distribution of HBV genotypes circulating among chronic hepatitis B patients reporting at the Korle-Bu Teaching Hospital (KBTH), Accra, Ghana.

Blood samples (10 ml) were collected from 250 consenting patients. DNA was extracted and amplified using polymerase chain reaction technique. Restriction fragment length polymorphism (RFLP) was used for the detection of genotypes.

Out of the 250 chronic hepatitis B patients who were HBsAg positive, 91 (36.4%) were males aged 29.8 ± 9.1 and 159 (63.6%) females aged 33± 12.1 years. HBV DNA was detected in 111 (44.4%) but only 58 (52%) of these were typeable. These were classified as genotype A, 8 (7.2%); genotype D, 3 (2.7%) and genotype E, 47 (42.3%). Our results did not show any association between the infecting genotype and age (X²= 0.923; p-value=0.623) or gender (X²= 0.283, p= 0.579).

Consistent with similar studies worldwide, the results suggest that genotypes A, D and E were the genotypes circulating among chronic hepatitis B patients who reported to the Korle-Bu Teaching Hospital with genotype E being the most predominant and therefore constitutes an important public health concern. We recommend further epidemiological studies to understand the implication of genotype E in terms of disease progression and treatment.

• Hepatitis B Virus
• chronic hepatitis B carriers
• hepatitis B genotype

• Argentina
• Bayesian coalescent analysis
• Hepatitis B virus
• Molecular epidemiology
• Phylogenetic analysis

HBV infection annually accounts for 1 million deaths worldwide as a result of cirrhosis, liver failure, and hepatocellular carcinoma. In addition to varying responses to antiviral therapy, HBV genotypes have also been shown to be associated with different pattern of disease progression. Despite a high HBV prevalence of >8 %, very few studies have been carried out in Cameroon to determine the genotype distribution across the country. The aim of this study was to determine the prevalent genotypes, level of viraemia and correlate these parameters with liver enzymes known to be the most affordable and widely used biomarkers for monitoring disease progression in Cameroon.

This was a hospital-community based study in which 81 participants who had been previously diagnosed of HBV were recruited and screened for HIV, HCV (for exclusion) and HBsAg for confirmation. Fifty known negative cases for HIV, HBV and HCV were tested and recruited to be used as healthy controls. Viral load and genotyping was performed only for HBV-mono infected cases using the Abbott RealTime HBV automated m2000 system and INNO-LiPA HBV Genotyping assay respectively. Liver enzymes were measured by spectrophotometry on both hepatitis B positive and healthy control cases.

The mean alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were significantly higher (p < 0.001) in HBV infected patients than “healthy controls”. Of the 81 HBV infected cases viral load was detected in 76 (93.8 %) with mean viral load of 120,807 IU/ml ± 440,159 SD. Mean viral load was significantly different in patients with abnormal AST and ALT when compared with patients who had normal ALT and AST. The identified genotypes in order of prevalence were A (47.4 %), E (39.5 %), C/E (3.9 %) A/C (2.6 %), A/E (2.6 %), B (1.3 %), A/B (1.3 %) and B/C (1.3 %).

Genotype E was significantly associated with higher mean viral load and mean AST levels. However, aminotransferase levels may not be a good marker for HBV disease progression as some patients could have normal levels but still present with very high viral loads and therefore, remain active HBV infection with possible high transmission.

• Asymptomatic Infection
• Hepatitis Delta Virus
• Prevalence
• Risk Factors
• Tunisia

• G1896A
• Genotype
• Hepatitis B
• Liver Cirrhosis
• Precore

The hepatitis B virus (HBV) is a global public health problem with more than 240 million people chronically infected worldwide, who are at risk for end-stage liver disease and hepatocellular carcinoma. There are an estimated 600000 deaths annually from complications of HBV-related liver disease. Antiviral therapy with nucleos/tide analogs (NA) targeting the HBV polymerase (P) can inhibit disease progression by long-term suppression of HBV replication. However, treatment may fail with first generation NA therapy due to the emergence of drug-resistant mutants, as well as incomplete medication adherence. The HBV replicates via an error-prone reverse transcriptase leading to quasispecies. Due to overlapping open reading frames mutations within the HBV P can cause concomitant changes in the HBV surface gene (S) and vice versa. HBV quasispecies diversity is associated with response to antiviral therapy, disease severity and long-term clinical outcomes. Specific mutants have been associated with antiviral drug resistance, immune escape, liver fibrosis development and tumorgenesis. An understanding of HBV variants and their clinical relevance may be important for monitoring chronic hepatitis B disease progression and treatment response. In this review, we will discuss HBV molecular virology, mechanism of variant development, and their potential clinical impact.

• Molecular virology
• Genetic heterogeneity
• Quasispecies
• Drug resistance
• Immune escape
• Viral lymphotropism
• Hepatitis B virus

Hepatitis B virus (HBV) is one of the important global health problems today. Infection with HBV can lead to a variety of clinical manifestations including severe hepatic complications like liver cirrhosis and hepatocellular carcinoma. Presently, routine HBV screening and diagnosis is primarily based on the immuno-detection of HBV surface antigen (HBsAg). However, identification of HBV DNA positive cases, who do not have detectable HBsAg has greatly encouraged the use of nucleic acid amplification based assays, that are highly sensitive, specific and are to some extent tolerant to sequence variation. In the last few years, the field of HBV molecular diagnostics has evolved rapidly with advancements in the molecular biology tools, such as polymerase chain reaction (PCR) and real-time PCR. Recently, apart of PCR based amplification methods, a number of isothermal amplification assays, such as loop mediated isothermal amplification, transcription mediated amplification, ligase chain reaction, and rolling circle amplification have been utilized for HBV diagnosis. These assays also offer options for real time detection and integration into biosensing devices. In this manuscript, we review the molecular technologies that are presently available for HBV diagnostics, with special emphasis on isothermal amplification based technologies. We have also included the recent trends in the development of biosensors and use of next generation sequencing technologies for HBV.

• Hepatitis B virus
• Polymerase chain reaction
• Isothermal amplification
• Real time polymerase chain reaction
• Biosensors
• Next generation sequencing

• Biosensing Techniques/trends
• DNA, Viral/blood
• DNA, Viral/genetics
• Genetic Markers
• Hepatitis B/blood
• Hepatitis B/diagnosis
• Hepatitis B/virology
• Hepatitis B Antibodies/blood
• Hepatitis B Surface Antigens/blood
• Hepatitis B virus/genetics
• Hepatitis B virus/immunology
• High-Throughput Nucleotide Sequencing/trends
• Humans
• Ligase Chain Reaction/trends
• Microfluidic Analytical Techniques/trends
• Molecular Diagnostic Techniques/trends
• Oligonucleotide Array Sequence Analysis/trends
• Predictive Value of Tests
• Prognosis
• Real-Time Polymerase Chain Reaction/trends
• Self-Sustained Sequence Replication/trends
• Viral Load

Hepatitis B virus (HBV) infection is a serious clinical problem worldwide. Conventional interferon (IFN)-α has been approved for the treatment of chronic hepatitis B (CHB). Short-term studies have demonstrated that IFN-based therapy is moderately effective in inducing the loss of hepatitis e antigen (HBeAg) or seroconversion (30%-40%) in HBeAg-positive patients and also produces sustained HBV DNA suppression (20%-30%) in HBeAg-negative patients. Many studies have reported a correlation between the HBV genotype and response to IFN treatment. The highest response rate to IFN treatment was found in patients infected with HBV genotype A, followed by HBV genotypes B, C, and D. The long-term effect of IFN-α on CHB has not yet been elucidated. The ability of IFN-α treatment to prevent new cirrhosis, complications associated with cirrhosis, and development of hepatocellular carcinoma (HCC) is controversial. The beneficial effect of IFN-α treatment in reducing the development of HCC has mainly been observed in treatment responders who already have cirrhosis. These inconsistent findings may be attributed to the inevitable limitations of comparisons across studies, including differences in the baseline characteristics of the study and the moderate suppression of HBV replication by IFN-α relative to nucleoside/nucleos(t)ide analogs.

• Chronic hepatitis B
• Hepatitis B virus
• Interferon α
• Long-term outcome
• Hepatocellular carcinoma

• Antiviral Agents/therapeutic use
• Biomarkers/blood
• Carcinoma, Hepatocellular/prevention & control
• Carcinoma, Hepatocellular/virology
• DNA, Viral/blood
• Disease Progression
• Genotype
• Hepatitis B e Antigens/blood
• Hepatitis B virus/drug effects
• Hepatitis B virus/genetics
• Hepatitis B virus/immunology
• Hepatitis B, Chronic/complications
• Hepatitis B, Chronic/diagnosis
• Hepatitis B, Chronic/drug therapy
• Hepatitis B, Chronic/virology
• Humans
• Interferon-alpha/therapeutic use
• Liver Cirrhosis/prevention & control
• Liver Cirrhosis/virology
• Liver Neoplasms/prevention & control
• Liver Neoplasms/virology
• Risk Factors
• Time Factors
• Treatment Outcome
• Viral Load
• Virus Replication

• genotype
• globalization
• hepatitis B virus
• nucleotide sequence
• recombination

• HBV
• HCC
• Nucleos(t)ide analogs

• genotype I
• hepatitis B virus
• mutation
• occult
• sequencing

Hepatitis B virus (HBV) infection is a public health problem as a cause of liver diseases including hepatocellular carcinoma and cirrhosis. It is estimated that 350 million people live with chronic infection and about one million people die every year from complication of this chronic disease in the world. So far, ten HBV genotypes (A-J) has been identified which show a geographical distribution. Throughout the world, carrier variability rate for hepatitis B infection is estimated to be 0.1% to 20%, with regions classified as having low endemicity (<2%), intermediate endemicity (2-7%) and high endemicity (>8%). The prevalence of hepatitis B infection is estimated at 2 to 7 percent In Iran. After HBV vaccination program the prevalence of hepatitis B infection has been reported less than 2%, so Iran can be considered one of the countries with low HBV infection endemicity. In Iran several studies were shown that the only genotype of HBV(100%)was found genotype D as the prominent type in some provinces, but some studies reported genotype B(5%)as well as genotype D(95%).The distribution of HBV genotypes may guide us in determining disease burden, prognosis and antiviral responses. So, it is important to know the epidemiologically of HBV genotyping as well.

• HBV
• cirrhosis
• hepatocellular carcinoma

• Genotyping Techniques
• Hepatitis B, Chronic
• Polymerase Chain Reaction

• Iran
• Persian Gulf
• full-length genome
• hepatitis B virus
• subgenotype
• subtype

• Drug Resistance
• Gene Products, pol
• Genotype
• Hepatitis B
• Lamivudine
• Mutation

• Direct Sequencing
• Genotype
• Hepatitis B Virus
• Restriction Fragment Length Polymorphism

• Hepatitis B Virus
• Liver Failure
• Mutation
• Risk Factors

Hepatitis B virus is hyperendemic in Sudan. Our aim was to molecularly characterize hepatitis B virus from Sudanese individuals, with and without liver disease, because genotypes play an important role in clinical manifestation and treatment management.

Ninety-nine patients - 30 asymptomatic, 42 cirrhotic, 15 with hepatocellular carcinoma, 7 with acute hepatitis and 5 with chronic hepatitis- were enrolled. Sequencing of surface and basic core promoter/precore regions and complete genome were performed.

The mean ± standard deviation, age was 45.7±14.8 years and the male to female ratio 77:22. The median (interquartile range) of hepatitis B virus DNA and alanine aminotransferase levels were 2.8 (2.2-4.2) log IU/ml and 30 (19–49) IU/L, respectively. Using three genotyping methods, 81/99 (82%) could be genotyped. Forty eight percent of the 99 patients were infected with genotype D and 24% with genotype E, 2% with putative D/E recombinants and 7% with genotype A. Patients infected with genotype E had higher frequency of hepatitis B e antigen-positivity and higher viral loads compared to patients infected with genotype D. Basic core promoter/precore region mutations, including the G1896A in 37% of HBeAg-negative individuals, could account for hepatitis B e antigen-negativity. Pre-S deletion mutants were found in genotypes D and E. Three isolates had the vaccine escape mutant sM133T.

Sudanese hepatitis B virus carriers were mainly infected with genotypes D or E, with patients infected with genotype E having higher HBeAg-positivity and higher viral loads. This is the first study to molecularly characterize hepatitis B virus from liver disease patients in Sudan.

• basal core promoter mutations
• chronic hepatitis B virus infection
• core mutations
• hepatitis B virus
• precore mutations

• Adult
• Aspartate Aminotransferases/blood
• Biomarkers/metabolism
• DNA Primers/genetics
• Enzyme-Linked Immunosorbent Assay
• Female
• HIV Infections/complications
• HIV Infections/epidemiology
• HIV Infections/transmission
• Hepatitis B/complications
• Hepatitis B/epidemiology
• Hepatitis B/transmission
• Hepatitis B virus/genetics
• Humans
• Liver Cirrhosis/etiology
• Liver Cirrhosis/pathology
• Male
• Prevalence
• Real-Time Polymerase Chain Reaction
• Rural Population
• Serologic Tests
• South Africa/epidemiology
• Statistics, Nonparametric