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In a trial of patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B, 24 week post-treatment biochemical and virological response rates with peginterferon alpha-2a with or without lamivudine were significantly higher than with lamivudine alone. The effect of pre-treatment factors on post-treatment responses was investigated. Multivariate analyses were performed using available data from 518 patients treated with peginterferon alpha-2a with or without lamivudine, or with lamivudine alone. A post-treatment response was defined as alanine aminotransferase (ALT) normalisation and hepatitis B virus (HBV) DNA level of <20,000 copies/ml. In logistic regression analyses across all treatment arms, peginterferon alpha-2a (with or without lamivudine) therapy, younger age, female gender, high baseline ALT, low baseline HBV DNA and HBV genotype were identified as significant predictors of combined response at 24 weeks post-treatment. In the peginterferon alpha-2a and lamivudine monotherapy arms, patients with genotypes B or C had a higher chance of response than genotype D infected patients (p<0.001), the latter responding better to the combination than to peginterferon alpha-2a monotherapy (p = 0.015). At 1 year post-treatment, response rates by intention-to-treat analysis were 19.2% for the peginterferon alpha-2a, 19.0% for the combination, and 10.0% for the lamivudine groups, with genotypes B or C associated with a sustained combined response to peginterferon alpha-2a with or without lamivudine therapy. Baseline ALT and HBV DNA levels, patient age, gender, and infecting HBV genotype significantly influenced combined response at 24 weeks post-treatment, in patients treated with peginterferon alpha-2a and/or lamivudine. At 1 year post-treatment HBV genotype was significantly predictive of efficacy for patients treated with peginterferon alpha-2a with or without lamivudine.

Hepatitis B virus (HBV) infection is endemic in South Africa however, there is limited data on the degree of liver disease and geographic variation in HIV/HBV coinfected individuals. In this study, we analysed data from the CIPRA-SA 'Safeguard the household study' in order to assess baseline HBV characteristics in HIV/HBV co-infection participants prior to antiretroviral therapy (ART) initiation. 812 participants from two South African townships Soweto and Masiphumelele were enrolled in a randomized trial of ART (CIPRA-SA). Participants were tested for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and HBV DNA. FIB-4 scores were calculated at baseline. Forty-eight (5.9%) were HBsAg positive, of whom 28 (58.3%) were HBeAg positive. Of those with HBV, 29.8% had an HBV DNA<2000 IU/ml and ALT<40 IU/ml ; 83.0% had a FIB-4 score <1.45, consistent with absent or minimal liver disease. HBV prevalence was 8.5% in Masiphumelele compared to 3.8% in Soweto (relative risk 2.3; 95% CI: 1.3-4.0). More participants in Masiphumelele had HBeAg-negative disease (58% vs. 12%, p = 0.002) and HBV DNA levels ≤2000 IU/ml, (43% vs. 6% p<0.007). One third of HIV/HBV co-infected subjects had low HBV DNA levels and ALT while the majority had indicators of only mild liver disease. There were substantial regional differences in HBsAg and HbeAg prevalence in HIV/HBV co-infection between two regions in South Africa. This study highlights the absence of severe liver disease and the marked regional differences in HIV/HBV co-infection in South Africa and will inform treatment decisions in these populations.

Perinatal hepatitis B virus (HBV) infection carries a significant risk of chronicity and complications while making infected people reservoirs for further transmission. Hepatitis B immunization in infants, with or without hepatitis B immune globulin (HBIG), has proven effective in preventing mother-to-child transmission. Nevertheless, some newborns of mothers with high viremia testing positive for hepatitis B e antigen (HBeAg) may not benefit from HBV immunoprophylaxis. Nineteen (10.2 %) of 186 infants born to HBV-infected mothers were HBV DNA-positive. HBV genotypes, serotypes, and hepatitis B surface antigen (HBsAg) sequences were comparable in most mother-cord blood-infant sample pairings, indicating that the infants' HBV strains originated from their mothers. Three (15.3 %) infants had overt HBV infection, whereas 16 (84.2 %) had occult HBV infection (OBI). The HBV isolates from infants exhibited 26 mutations: 38.5 % in the ‘a’ determinant and 61.5 % in the rest of HBsAg. Mutations were identified in B-cell and T-cell epitopes, impairing humoral and cellular responses to detect or neutralize the virus. This rendered immunoprophylaxis and diagnostics ineffective while inducing tolerance to the infection. HBV strains with these mutations can persist and cause complications, but they can be transmitted undetected by HBsAg tests commonly used in community healthcare. This study reveals the risk of HBV transmission from HBsAg mutant-infected mothers to newborns despite having received the birth dose with HBIG and complete hepatitis B vaccination. •HBV S protein mutation can impair detection and immune neutralization of the virus•HBV mutants can persist in fully vaccinated infants and spread unnoticed•Babies born to mothers infected with HBV mutants may not be prevented by vaccination and HBIG•Vaccine escape and diagnosis failure are challenges to the efficacy of vaccination

Hepatitis B virus (HBV) is a major cause of human hepatitis. There is considerable uncertainty about the timescale of its evolution and its association with humans. Here we present 12 full or partial ancient HBV genomes that are between approximately 0.8 and 4.5 thousand years old. The ancient sequences group either within or in a sister relationship with extant human or other ape HBV clades. Generally, the genome properties follow those of modern HBV. The root of the HBV tree is projected to between 8.6 and 20.9 thousand years ago, and we estimate a substitution rate of 8.04 × 10 −6 –1.51 × 10 −5 nucleotide substitutions per site per year. In several cases, the geographical locations of the ancient genotypes do not match present-day distributions. Genotypes that today are typical of Africa and Asia, and a subgenotype from India, are shown to have an early Eurasian presence. The geographical and temporal patterns that we observe in ancient and modern HBV genotypes are compatible with well-documented human migrations during the Bronze and Iron Ages 1 , 2 . We provide evidence for the creation of HBV genotype A via recombination, and for a long-term association of modern HBV genotypes with humans, including the discovery of a human genotype that is now extinct. These data expose a complexity of HBV evolution that is not evident when considering modern sequences alone. Phylogenies reconstructed using 12 hepatitis B virus genomes, which were recovered from ancient human genome data, reveal a complex history of hepatitis B evolution that is not evident when using only modern samples.

Occult Hepatitis B virus infection (OBI) is prevalent among high-risk and immunized populations in regions with high endemicity. OBI could be reactivated and/or transmitted, making it a significant risk factor for liver disease progression, including cirrhosis and hepatocellular carcinoma. This cross-sectional study was conducted on vaccinated children born to HBsAg positive mothers in the Esfandiar region of Iran. Families with a member who tested positive for HBV were included in the study. Blood samples were collected, and serological assays were performed to detect anti-HBc, HBsAg, anti-HBs, and HBeAg. Molecular examinations, including DNA extraction, PCR assays and real-time PCR quantification, were performed to identify OBI. Subsequently, the amplified segment of the S gene underwent DNA sequencing for mutations analysis and HBV genotyping. In total, 100 children were examined: Serological assessments indicated positive results for anti-HBs, anti-HBc, and HBsAg in 43%, 5%, and 2% of cases, respectively. PCR assays revealed 6.1% prevalence of OBI (95% CI: 0.013–0.11). Phylogenetic analysis confirmed that all isolates belonged to HBV genotype D and sub-genotype D1. Mutational analysis identified immune escape mutations in the HBsAg protein, including T45N, P105A, and Q129H. The findings suggest a suboptimal protective efficacy of the HBV vaccine in this highly endemic region. The presence of OBI among vaccinated individuals highlights the potential for transmission through congenital and perinatal routes. Screening of mothers and women of childbearing age, administration of HBV immunoglobulin, and reinforcement of Hepatitis B vaccination programs are imperative in such regions.

In 2011, a study on preventing mother-to-child transmission (PMTCT) of Hepatitis B virus (HBV) was conducted in Yunan province, China, and a child cohort was formed to assess PMTCT's long-term effectiveness. In 2022, subjects were randomly selected from this cohort to investigate HBV infection status and anti-HBs antibody levels among the HBsAg-negative children from the 2011 PMTCT group. HBV markers (HBsAg, anti-HBs, anti-HBc) and genomic information were detected, and risk factors for HBV breakthrough infection were analyzed. In total, 235 children were enrolled. HBsAg and anti-HBc positive rates were 1.7 % (4/235) and 5.96 % (14/235). HBsAg prevalence did not substantially increase, but four new HBV carriers were identified, with S gene sequences highly homologous to their parents'. The anti-HBs positive rate dropped significantly (from 86.38 % in 2011 to 58.30 % in 2022, χ2 = 46.32, P < 0.001), yet it went up among those who had booster vaccinations (93.2 % in 2022; 78.0 % in 2011), though antibody levels did not increase. Phylogenetic analysis confirmed the possible intrafamilial HBV transmission and no significant important mutations. Univariate and logistic regression analyses indicated that maternal HBeAg positivity were a major risk factors for children's HBV breakthrough infection (OR = 4.23, 95 % CI: 1.17–15.25). In conclusion, the positive rate and levels of anti-HBs antibodies have declined over time, but infection rates has not substantially increased. Children of HBsAg-positive parents remained at high risk of HBV breakthrough infection. Even with successful PMTCT, measures should be taken to maintain their immunity and reduce direct HBV exposure. •Eleven years after the birth, infants born to HBsAg-positive mothers had HBsAg and anti-HBc positivity rates of 1.70 % and 5.96 %, respectively, with no significant increase in HBsAg prevalence.•The positivity rate and titers of anti-HBs antibodies decreased over time, but positivity rate increased among those received booster vaccinations.•Evidence of intrafamilial transmission was observed, with no significant key mutations detected, and maternal HBeAg positivity identifying as a significant risk factor.

Background Despite extensive HBV vaccination efforts in Indonesia, the prevalence of occult hepatitis B virus infection (OBI) remains a concern, particularly among blood donors. This study investigated the prevalence of OBI, the distribution of circulating HBV genotypes, seropositivity for HBV-specific antibodies, and the potential influence of mutational characteristics on HBsAg secretion among blood donors in Jember, Indonesia. Methods A total of 330 HBsAg-negative blood donor samples from the Indonesian Red Cross in Jember were analyzed for HBV serological markers. Qualitative nested PCR and quantitative real-time PCR were used to detect HBV viral DNA and to measure viral load, respectively. HBV genotyping in positive samples was performed using Sanger sequencing of the S gene fragment. Results The analysis revealed an OBI prevalence of 3%. Serological testing indicated that 27% of participants were positive for anti-HBs antibodies, 18% for anti-HBc, and 6% for anti-HBc alone. All HBV DNA-positive cases belonged to genotype B, primarily sub genotypes B3 and B4. Phylogenetic analysis revealed multiple mutations in the HBV surface (S) gene and the reverse transcriptase (RT) domain of the polymerase (Pol) protein, including immune escape mutations, suggesting potential risks for HBV transmission and reactivation. Conclusions These findings emphasize the need for enhanced screening, including NAT alongside serological testing, to mitigate OBI risks in blood donors and improve transfusion safety and public health policies in HBV-endemic regions of Indonesia.

Hepatitis B virus (HBV) persists as a major global public health burden, with hyperendemic prevalence in sub-Saharan Africa. Populations with elevated exposure to percutaneous transmission risks, including incarcerated individuals and healthcare workers demonstrate heightened HBV susceptibility. Despite this, genomic data from Northeastern Kenya and Kenyan prison populations remain scarce. To characterize HBV genotypic diversity circulating in Northeastern Kenya, among low-risk (blood donors) and high-risk (prison inmates) populations. A cross-sectional investigation compared HBV seroprevalence and genotypes between incarcerated individuals (n = 130) and voluntary blood donors (n = 130) in Garissa County, Northeastern Kenya. Serum samples were subjected to Hepatitis B surface antigen (HBsAg) screening, PCR amplification of a 940-bp overlapping surface/polymerase gene, sequencing, and phylogenetic/recombination analyses of the resulting sequences. Seroprevalence was higher among incarcerated individuals (5.4%, 7/130) than blood donors (3.1%, 4/130). Hepatitis B Virus DNA was detected in 22 samples which were all successfully sequenced. Genotype D dominated both cohorts (81.8%), while genotype A sub genotype A1 occurred exclusively in incarcerated participants (18.2%). All genotype D strains were recombinants: D/A (61%) and D/E (39%). Sequences are accessible in GenBank (accession numbers: PV816552-PV816573). This first genomic study of HBV in Kenyan prisons confirms incarcerated populations as high-risk. The predominance of genotype D-an unusual finding in this region and high recombinant frequency (100% of genotype D strains) underscore significant viral evolution. Expanded genomic surveillance is imperative to define HBV diversity, inform vaccine efficacy monitoring, guide screening policies and optimize control strategies in Northeastern Kenya.

The immunopathogenesis and molecular mechanisms involved during a hepatitis B virus (HBV) infection have made the approaches for research complex, especially concerning the patients’ responses in the course of the early acute stage. The study of molecular bases involved in the viral clearance or persistence of the infection is complicated due to the difficulty to detect patients at the most adequate points of the disease, especially in the time lapse between the onset of the infection and the viral emergence. Despite this, there is valuable data obtained from animal and in vitro models, which have helped to clarify some aspects of the early immune response against HBV infection. The diversity of the HBV (genotypes and variants) has been proven to be associated not only with the development and outcome of the disease but also with the response to treatments. That is why factors involved in the virus evolution need to be considered while studying hepatitis B infection. This review brings together some of the published data to try to explain the immunological and molecular mechanisms involved in the different stages of the infection, clinical outcomes, viral persistence, and the impact of the variants of HBV in these processes.

Sequence heterogeneity is a feature of hepatitis B virus (HBV), the prototype member of the family Hepadnaviridae. Based on an intergroup divergence of greater than 7.5% across the complete genome, HBV has been classified phylogenetically into 9 genotypes, A-I, with a putative 10th genotype ‘J', isolated from a single individual. With between approximately 4 and 8% intergroup nucleotide divergence across the complete genome and good bootstrap support, genotypes A-D, F, H, and I are classified further into subgenotypes. There is a broad and highly statistically significant correlation between serological subtypes and genotypes, and in some cases, serological subtypes can be used to differentiate subgenotypes. The genotypes, and certain subgenotypes, have distinct geographical distributions and are important in both the clinical manifestation of infection and response to antiviral therapy. HBV genotypes/subgenotypes and genetic variability of HBV are useful in epidemiological and transmission studies, tracing human migrations, and in predicting the risk for the development of severe liver disease and response to antiviral therapy. Moreover, knowledge of the genotype/subgenotype is important in implementing preventative strategies. Thus, it is crucial that new strains are correctly assigned to their respective genotype/subgenotype and consistent, unambiguous, and generally accepted nomenclature is utilized.