Hepatitis B Virus Infection Research Articles

Monocyte Transcriptome in Different Phases of Chronic Hepatitis B Virus Infection Uncovers Potential Functional Roles.

The hepatitis B virus (HBV) chronic infection goes through different phases, i.e., immune tolerant (IT), immune clearance (IC), and inactive carrier (IN) resulting from the interplay of viral replication and immune response. Although the adaptive immune response is central to viral control, roles of the innate immune cells are less prominent. We explored monocyte transcriptome in these different phases of HBV infection to understand the nature of its involvement and identify unique differentially expressed genes (DEGs) in each phase. CD14+ peripheral blood monocytes were isolated from patients in the IT, IC, and IN phases and from healthy subjects and their RNA was sequenced. The significant DEGs were studied through gene annotation databases to understand differentially modulated pathways. The DEGs were further validated by qRT-PCR to identify genes that were uniquely expressed in each phase. It was found that TNFRSF12A was upregulated in all the HBV samples. The IN phase had six uniquely upregulated genes, i.e., PI3, EMP1, STX1A, RRAD, SPINK1, and SNORD3B-2. E2F7 was most consistently downregulated in the IT phase, and in the IC phase, IL23A and PI3 were specifically downregulated. Cut-off values were generated by ROC curve analysis to differentiate between the groups based on their expression levels. The monocyte functions are majorly suppressed in the IT and IC phases and are, however, somewhat metabolically active in the IN phase.

SATCAS: A CRISPR/Cas13a-based simultaneous amplification and testing platform for one-pot RNA detection and SNPs distinguish in clinical diagnosis

The clinical diagnosis of pathogen infectious diseases increasingly requires sensitive and rapid RNA detection technologies. The RNA-guided clustered regularly interspaced short palindromic repeats (CRISPR)/Cas13a system has shown immense potential in molecular diagnostics due to its trans-cleavage activity. However, most Cas13a-based detection methods require an amplicon transcription step, and the multi-step open-tube operations are prone to contamination, limiting their widespread application. Here, we propose an ultrasensitive (single-copy range, ∼aM) and rapid (within 40 min) isothermal one-pot RNA detection platform, termed SATCAS (Simultaneous Amplification and Testing platform based on Cas13a). This method effectively distinguishes viable bacteria (0%–100%) under constant total bacterial conditions, demonstrating its robustness and universality. SATCAS excels in identifying single nucleotide polymorphisms (SNPs), particularly detecting 0.5% drug-resistant mutations. We validated SATCAS by detecting infections in biological samples from 68 HBV, 23 EBV, and 48 SARS-CoV-2 patients, achieving 100% sensitivity, 92.86% specificity, and 97.06% accuracy in HBV infection testing. We anticipate that SATCAS has broad application potential in the early diagnosis, subtyping, drug resistance detection, and point-of-care monitoring of pathogen infectious diseases.

Sequential Peg-IFN after bepirovirsen may reduce post-treatment relapse in chronic hepatitis B

Bepirovirsen, an antisense oligonucleotide, induces sustained reductions in hepatitis B surface antigen (HBsAg) and HBV DNA to below the lower limit of quantification (<LLOQ) in a subset of patients. The B-Together study investigated if sequential bepirovirsen and pegylated interferon-α-2a (Peg-IFN) therapy can reduce relapse rates and improve response rates. In this phase IIb, multicentre, open-label trial, participants on stable nucleos(t)ide analogue (NA) therapy were randomised 1:1 to bepirovirsen 300mg once weekly (plus loading dose on Days 4 and 11) for 24 (Arm 1) or 12 (Arm 2) weeks followed by Peg-IFN 180μg once weekly for up to 24 weeks, with up to 36 weeks follow-up. Participants continued NA therapy throughout. The primary outcome was the proportion of participants with HBsAg <0.05 IU/ml and HBV DNA <LLOQ for 24 weeks after planned end of Peg-IFN treatment, in the absence of newly initiated antiviral therapy. The intent-to-treat population included 108 participants (Arm 1, n= 55; Arm 2, n= 53). The primary outcome was achieved by 5 (9%) participants in Arm 1 and 8 (15%) in Arm 2. All responders had baseline HBsAg ≤3,000 IU/ml. Indirect comparison with the phase IIb study B-Clear indicates that sequential addition of Peg-IFN may reduce the relapse rates previously observed with bepirovirsen alone. The proportions of participants with adverse events and treatment-related adverse events in both treatment windows were similar between treatment arms. Sequential therapy with bepirovirsen followed by Peg-IFN is tolerable and effective in participants with chronic HBV infection on stable NA therapy. This proof-of-concept trial demonstrates a potential strategy to extend responses to bepirovirsen by reducing relapse. This phase IIb study investigated whether sequential therapy with bepirovirsenfollowed by Peg-IFN could improve off-treatment response rates to bepirovirsen alone by converting partial bepirovirsen responders to full responders and/or reducing relapse rates in participants with chronic HBV. These data show that sequential therapy with bepirovirsen followed by Peg-IFN is tolerable and effective; in patients with a bepirovirsen response, sequential treatment with Peg-IFN may help to reduce off-treatment relapses in participants on stable NA. Participants had a similar response during bepirovirsen treatment as seen in B-Clear, with increased response rates in participants with lower baseline HBsAg; all responders to the sequential regimen had baseline HBsAg <3000 IU/mL. As the first study of antisense oligonucleotide-mediated RNA silencing followed by interferon immunomodulation in patients with chronic HBV infection, this study is an important proof-of-concept for sequential therapy, shedding light on the therapeutic potential of utilising immunomodulators following suppression of HBV antigens. NCT04676724.

The Prevalence and Molecular Epidemiology of Hepatitis Delta Virus in Nigeria: The Results of a Nationwide Study.

Hepatitis delta virus (HDV) is a satellite of hepatitis B virus (HBV), which requires the HBV surface antigen (HBsAg) for its assembly and propagation. Although countries affected by HBV infection in Africa are well identified, data on HDV infection are still scarce, like in Nigeria, where HBV infection is endemic. In this study, we aimed to determine the prevalence of HDV infection and identify the circulating genotypes/strains in the country. A nationwide study was performed on 1281 HBsAg-positive samples collected from patients across eleven sites drawn from the six geopolitical zones in Nigeria. Anti-HDV antibody (HDV-Ab) screening and HDV-RNA viral load quantification were performed using a commercial ELISA assay and real-time RT-PCR kit, respectively. HDV genotyping was performed by the Sanger sequencing of amplicons from the so-called R0 region of the viral genome, followed by phylogenetic analyses. Of the 1281 HBsAg-positive samples, 61 (4.8%) were HDV-Ab positive, among which, 12 (19.7%) were HDV-RNA positive. Genotypes were obtained for nine of them: seven "African" HDV-1, one "Asian/European" HDV-1 and one HDV-6. This study shows that Nigeria is a country of low HDV prevalence where mainly "African" genotype-1 strains are circulating.

Interferon-stimulated gene (ISG12a) suppresses hepatitis B virus replication in Huh 7 cells line

Hepatitis B virus (HBV) and its associated chronic liver disease pose a significant health hazard. Chronic HBV infection is a major contributor to the development of liver cirrhosis, liver fibrosis, and liver cancer. This study focused on ISG12a and its inhibitory effect in Huh7 cells on HBV gene expression and replication. The mammalian hepatoma cells Huh7 were transfected with the pHBV1.3 vector (pCAGGS) or HA-tagged ISG12a to determine the overexpression, to test this hypothesis further, we did knockdown or silencing by transducing Huh7 cells with lentiviruses containing shRNAs targeting ISG12a or scramble control shRNA (shControl). The expression of ISG12a was evaluated through western blot analysis. The HBsAg and HBeAg secretion in the Huh7 cells’ culture media was examined using an ELISA test. The qRT-PCR confirmed the mRNA and 3.5 mRNA Kb of ISG12a. The HBV total RNA was extracted and evaluated through a Northern blot. The isolated DNA was detected through qPCR. Additionally, a mechanistic study of enhancer II (EnhII/Cp) was examined through luciferase reporter testing. Our research findings indicate that ISG12a, an interferon-stimulated gene (ISG), plays a crucial role in suppressing the replication and gene expression of HBV. According to our study using the Huh7 cell system, overexpression of ISG12a resulted in a notable reduction in HBV protein levels as well as intracellular core-associated DNA and RNA levels. On the other hand, silencing ISG12a in Huh7 cells resulted in increased HBV RNA transcripts, DNA, and secreted proteins, indicating that ISG12a plays a role in suppressing HBV replication. Additionally, the research revealed that ISG12a inhibits the function of the EnhII/Cp promoter, which results in reduced HBV gene expression. The EnhII/Cp promoter is involved in regulating HBV gene expression, and the study showed that ISG12a restricts its activity. ISG12a may have a regulatory role in controlling the expression of HBV genes. These findings highlight the importance of ISG12a in HBV gene expression and provide valuable insights for understanding its antiviral function.

Both middle and large envelope proteins can mediate neutralization of hepatitis B virus infectivity by anti-preS2 antibodies: escape by naturally occurring preS2 deletions.

Hepatitis B virus (HBV) expresses co-terminal large (L), middle (M), and small (S) envelope proteins containing preS1/preS2/S, preS2/S, and S domain alone, respectively. S and preS1 domains mediate sequential virion attachment to heparan sulfate proteoglycans and sodium taurocholate cotransporting polypeptide (NTCP), respectively, which can be blocked by anti-S and anti-preS1 antibodies. How anti-preS2 antibodies neutralize HBV infectivity remains enigmatic. The late stage of chronic HBV infection often selects for mutated preS2 translation initiation codon to prevent M protein expression, or in-frame preS2 deletions to shorten both L and M proteins. When introduced to infectious clone of genotype C or D, both M-minus mutations and most 5' preS2 deletions sustained virion production. Such mutant progeny viral particles were infectious in NTCP-reconstituted HepG2 cells. Neutralization experiments were performed on the genotype D clone. Although remaining susceptible to anti-preS1 and anti-S neutralizing antibodies, M-minus mutants were only partially neutralized by two anti-preS2 antibodies tested while preS2 deletion mutants were resistant. By infection experiments using viral particles with lost versus increased M protein expression, or a neutralization escaping preS2 deletion only present on L or M protein, we found that both full-length L and M proteins contributed to virus neutralization by the two anti-preS2 antibodies. Thus, immune escape could be a driving force for the selection of M-minus mutations, and especially preS2 deletions. The fact that both L and M proteins could mediate neutralization by anti-preS2 antibodies may shed light on the underlying molecular mechanism.IMPORTANCEThe large (L), middle (M), and small (S) envelope proteins of hepatitis B virus (HBV) contain preS1/preS2/S, preS2/S, and S domain alone, respectively. The discovery of heparan sulfate proteoglycans and sodium taurocholate cotransporting polypeptide (NTCP) as the low- and high-affinity HBV receptors could explain neutralizing potential of anti-S and anti-preS1 antibodies, respectively, but how anti-preS2 neutralizing antibodies work remains enigmatic. In this study, we found two M-minus mutants in the context of genotype D partially escaped two anti-preS2 neutralizing antibodies in NTCP-reconstituted HepG2 cells, while several naturally occurring preS2 deletion mutants escaped both antibodies. By point mutations to eliminate or enhance M protein expression, and by introducing preS2 deletion selectively to L or M protein, we found binding of anti-preS2 antibodies to both L and M proteins contributed to neutralization of wild-type HBV infectivity. Our finding may shed light on the possible mechanism(s) whereby anti-preS2 antibodies neutralize HBV infectivity.

Investigating the role of GTPase in inhibiting HBV replication and enhancing interferon therapy efficacy in chronic hepatitis B patients

BackgroundInterferon-alpha (IFNα) is a common treatment for chronic hepatitis B virus (HBV) infection, but its efficacy varies widely among patients. GTPASE, an interferon-stimulated gene (ISG), has recently been identified as a factor in antiviral immunity, though its role in HBV infection is not fully understood. ObjectiveThis study investigates the role of GTPASE in enhancing the antiviral effects of IFNα against HBV and elucidates its mechanism of action. MethodsWe analyzed the impact of GTPASE overexpression and silencing on HBV replication and clearance in HBV-infected cells. Molecular docking studies assessed the interaction between GTPASE and HBV surface antigens (HBs). Clinical samples from HBV patients undergoing Peg-IFNα treatment were also evaluated for GTPASE expression and its correlation with treatment efficacy. ResultsOverexpression of GTPASE led to significant inhibition of HBV replication, increased HBeAg seroconversion, and enhanced HBsAg clearance. GTPASE directly bound to HBs proteins, reducing their levels and affecting viral particle formation. Silencing GTPASE reduced these effects, while combined treatment with Peg-IFNα and GTPASE overexpression further improved antiviral outcomes. Mutational analysis revealed that specific sites in GTPASE are crucial for its antiviral activity. ConclusionsGTPASE acts as a positive regulator in IFNα-induced antiviral immunity against HBV. It enhances the therapeutic efficacy of IFNα by targeting HBs and modulating viral replication. GTPASE levels may serve as a predictive biomarker for response to Peg-IFNα therapy, highlighting its potential for improving individualized treatment strategies for chronic HBV infection.

Epidemiology, Natural History, and Outcome of Chronic Hepatitis B in Children

Abstract Hepatitis B virus (HBV) infection is a global epidemic whose prevention and control among children warrant significant attention. Despite the availability of effective vaccines, the disease continues to affect millions of children worldwide, underscoring the need for a comprehensive understanding of its epidemiology and natural history in this vulnerable population. While research on HBV in adults has advanced considerably, the natural history of HBV infection in children remains less well-defined and may differ from adult studies due to unique immunological and physiological characteristics. This article reviews the epidemiological characteristics of HBV infection in children worldwide and summarizes the research progress on the natural outcomes of children with chronic HBV infection. Furthermore, the necessity of this review stems from the critical role that early detection, monitoring, and timely intervention play in mitigating the long-term consequences of chronic hepatitis B (CHB) in children. By synthesizing current evidence and identifying knowledge gaps, we hope to inform clinical practice, guide future research directions, and ultimately improve the health outcomes of children living with HBV. In doing so, this review article offers a valuable reference for healthcare providers, researchers, and policymakers working to combat the global challenge of HBV infection among children. The aim is to provide a relevant reference for the monitoring, screening, diagnosis, and treatment of children with CHB.

Seroprevalence of hepatitis B virus and hepatitis C virus infection among pregnant women attending antenatal care at Guhala Primary Hospital, Northwestern Ethiopia

BackgroundHepatitis B virus (HBV) and Hepatitis C Virus (HCV) infections are global issues that disproportionately affect developing countries. Pregnancy-related HBV and HCV infections are associated with a high risk of vertical transmission and complications for the mother as well as the newborn. Therefore, this study aims to determine the seroprevalence of hepatitis B virus and hepatitis C virus infection among pregnant women attending antenatal care at Guhala Primary Hospital, Northwestern Ethiopia.MethodsA hospital-based retrospective study was conducted from July to September 2022 on HBV and HCV registered books from September 1, 2017, to August 30, 2019, for a year. The presence of HBsAg and anti-HCV in serum was detected using the One Step Cassette Style HBsAg and anti-HCV antibody test kit. Data were analyzed using SPSS version 26 software.ResultsIn this study, a total of 2252 participants for HBsAg and 538 participants for ant-HCV rapid tests of records in the laboratory logbook were included. The mean age of the study participants was 25.6years (± 5.8SD). The overall prevalence of HBsAg and anti-HCV was 6.0% (134/2252) and 2.4% (13/538), respectively. There were 0.4% (2/538) coinfection results between HBV and HCV among pregnant women.Conclusion and recommendationIn this study, intermediate seroprevalence of HBV and HCV infection was detected among pregnant women attending antenatal care. The Hepatitis B virus was predominantly higher among pregnant women aged between 25 and 34 years. To manage and stop the potential vertical transmission of these viral agents during the early stages of pregnancy, routine prenatal testing for HBV and HCV infections should be taken into consideration.

Prevalence and viral suppression of hepatitis B virus infection among people living with HIV on antiretroviral therapy in Sierra Leone

ObjectiveSub-Saharan Africa is one of the regions with the highest burdens of HIV and hepatitis B virus (HBV), but data on the impact of antiretroviral therapy (ART) on HBV DNA...

Interleukin-8 in HepG2 cells: Enhancing antiviral proteins in uninfected cells but promoting HBV replication in infected cells

In vitro studies have revealed that hepatitis B virus (HBV) infection upregulates interleukin-8 (IL-8), which enhances HBV replication. Clinically, elevated IL-8 levels in chronic HBV patients are associated with diminished therapeutic efficacy of interferon-α (IFN-α). Our study advances these findings by demonstrating that IL-8 promotes the expression of myxovirus resistance A (MxA) and protein kinase R (PKR) in HepG2 cells via the PI3K-AKT pathway. However, HBV-infected cells fail to exhibit IL-8-induced upregulation of MxA and PKR, likely due to HBV's upregulation of PP2A that inhibits the PI3K-AKT pathway. Notably, IL-8 targets the C/EBPα transcription factor, increasing HBV promoter activity and viral replication, which in turn partially suppresses the expression of MxA and PKR induced by IFN-α. Our findings uncover a mechanism by which HBV may evade immune responses, suggesting potential new strategies for immunotherapy against chronic HBV infection.

Hepatitis B: A Pilot study on awareness and attitude among staff nurses and students of a teaching hospital in India.

Hepatitis B is a serious public health concern and health care professionals especially nurses are at higher risk of acquiring this infection. Basic knowledge, awareness and a positive attitude are required to prevent this disease. The present pilot study was conducted to assess awareness and attitude regarding hepatitis B among staff nurses and nursing students of a teaching hospital in north India. A total of 205 subjects who gave consent to participate were included in this descriptive study. A self-structured pre-tested close ended questionnaire comprising of two parts was used to collect information from the study subjects. First part collected information on demographic details of the study subject and second part assessed subjects' awareness and attitude on various aspects of hepatitis B infection including vaccination. Chi-square test and multiple linear regression analysis was used for statistical analysis. The mean age of the study subjects was 25.8±5.6 years. Awareness regarding HBV infection was present among 92.6% (190) of subjects. Long-term effects of hepatitis B were known to 58.4% (119) of subjects and 79.1% (162) of subjects reported taking universal precautions. Half of the subjects (105), were getting regularly tested for hepatitis B antigen.The odds of getting regularly tested for hepatitis B antigen were 3.26 times greater in female subjects and 3.45 times greater in subjects who were GNMs. Low awareness levels were reported regarding some important aspects of hepatitis B among study subjects though more than 90% were aware of it. There is an urgent need for education and training programs for nurses designed to increase their knowledge about HBV infection.

Progress Toward Elimination of Mother-to-Child Transmission of Hepatitis B Virus - Region of the Americas, 2012-2022.

In 2022, an estimated 5 million persons in the World Health Organization Region of the Americas (AMR) were living with chronic hepatitis B virus (HBV) infection, the leading cause of hepatocellular carcinoma and cirrhosis worldwide. Most chronic infections are acquired through mother-to-child transmission (MTCT) or horizontal transmission during childhood and are preventable with hepatitis B vaccination, including a birth dose (HepB-BD), followed by 2-3 additional doses (HepB3) in infancy. The Pan American Health Organization (PAHO) Elimination of MTCT of HBV infection strategy is intended to reduce chronic HBV infection (measured by hepatitis B surface antigen [HBsAg] seroprevalence) to ≤0.1% among children by achieving 1) ≥95% coverage with HepB-BD and HepB3; and 2) ≥80% of pregnant women received testing for HBsAg, and provision of hepatitis B immunoglobulin to HBV-exposed neonates. By 2012, all 51 AMR countries and territories (countries) provided HepB3 nationwide, and by 2021, 34 (67%) provided HepB-BD nationwide. Mathematical models estimate that HBsAg seroprevalence in children is ≤0.1% in 14 (28%) of 51 countries and at the regional level. Three (6%) of 51 countries met the 95% coverage targets for both HepB3 and HepB-BD during both 2021 and 2022. Of these, two have likely met criteria for the elimination of MTCT of HBV infection. However, in 2022, HepB3 coverage had declined by ≥10 percentage points in 15 (37%) of 41 countries with 2012 coverage data for comparison. These declines in HepB3 coverage, as well as the absence of HepB-BD in the routine immunization schedules in 17 countries, threaten PAHO's progress toward the elimination of MTCT of HBV infection. Efforts to introduce HepB-BD and maintain high HepB3 and HepB-BD coverage are needed.

The impact of donor hepatitis B virus infection on transplant outcomes in deceased donor kidney transplantation recipients.

The use of hepatitis B virus (HBV)-positive donor kidneys to expand the donor pool has been implemented, but limited evidence exists regarding their impact on transplant outcomes. This study aimed to investigate the effects of donor HBV infection on transplant outcomes. Donor and recipient data between 2015 and 2021 were collected. A total of 743 kidney transplant cases were screened, including 94 donor hepatitis B surface antigen (HBsAg)+/recipient HBsAg- (D+R-) and 649 donor HBsAg-/recipient HBsAg- (D-R-) cases. The analysis endpoints included recipient HBV infection, delayed graft function (DGF), peak estimated glomerular filtration rate (eGFR) within 12 months, recipient survival, and death-censored graft survival (DCGS). The D+R- group had a significantly higher risk of HBV infection compared to the D-R- group (6/72 vs. 3/231; relative risk, 6.4; p = 0.007). The risk of HBV transmission decreased significantly with increasing hepatitis B surface antibody (HBsAb) titer (p for trend = 0.003). Furthermore, the D+R- group did not exhibit an increased risk of DGF compared to the D-R- group (odds ratio, 0.70; p = 0.51) in the multivariable mixed model. Both groups had similar peak eGFR within 12 months (β = 1.01, p = 0.71), and this had no impact on patient survival (hazard ratio [HR], 0.36; p = 0.10) and DCGS (HR, 0.79, p = 0.59) in the shared-frailty Cox model. The use of HBsAg-positive donor kidneys appears relatively safe for HBV-immunized recipients in the short term. D+R- does not negatively affect graft function recovery and provides comparable posttransplant outcomes. Maintaining an HBsAb titer over 100 IU/L before transplantation is critical to reduce the risk of HBV transmission.

Identification of amino acids restricting HBV receptor function in porcine NTCP

With 254 million chronically infected patients, hepatitis B virus (HBV) continues to be a severe health threat. While animal models play a crucial role in developing new therapies, the availability of preclinical HBV models is very limited. Therefore, novel in vivo infection models are urgently needed. The bona fide HBV receptor, sodium-taurocholate cotransporting polypeptide (NTCP), determines HBV’s species and cell-type specificity. Recent studies have indicated that the expression of human NTCP is the only limiting factor for HBV infection in selected species, such as macaques or pigs. Here, we confirm HBV infection of pig hepatocytes expressing human NTCP and show that porcine NTCP does not support HBV binding. By gradually humanizing porcine NTCP and site-directed mutagenesis, we identified amino acids 158 and 167 in porcine NTCP, limiting HBV interaction. In a proof-of-concept experiment, we showed that the expression of porcine NTCP with humanized amino acids 157-167 renders primary porcine hepatocytes fully susceptible to HBV. These results pave the way for generating transgenic pigs with humanized porcine chimeric NTCP as a novel, fully immunocompetent infection model for developing and validating new curative HBV therapies.

Modelling the potential impact of global hepatitis B vaccination on the burden of chronic hepatitis B in the United States.

About 80% of persons with chronic hepatitis B virus (HBV) infection in the United States are non-US-born. Despite improvements in infant hepatitis B vaccination globally since 2000, work remains to attain the World Health Organization's (WHO) global 2030 goal of 90% vaccination. We explore the impacts on the United States of global progress in hepatitis B vaccination since 2000 and of achieving WHO hepatitis B vaccination goals. We simulated immigrants with HBV infection arriving to the United States from 2000 to 2070 using models of the 10 countries from which the largest numbers of individuals with HBV infection were born. We estimated costs in the United States among these cohorts using a disease simulation model. We simulated three scenarios: a scenario with no progress in infant vaccination for hepatitis B since 2000 (baseline), current (2020) progress and achieving WHO 2030 goals for hepatitis B vaccination. We estimate current hepatitis B vaccination progress since the 2000 baseline in these 10 countries will lead to 468,686 fewer HBV infections, avoid 35,582 hepatitis B-related deaths and save $4.2 billion in the United States through 2070. Achieving the WHO 2030 90% hepatitis B infant vaccination targets could lead to an additional 16,762 fewer HBV infections, 989 fewer hepatitis B-related deaths and save $143 million through 2070. Global hepatitis B vaccination since 2000 reduced prevalence of HBV infection in the United States. Achieving the WHO 2030 infant vaccination goals globally could lead to over one hundred million dollars in additional savings.

Seroprevalence of Hepatitis B Virus among Blood Donors at National Blood Transfusion and Research Center-Taiz Branch, Yemen

Hepatitis B Virus (HBV) represents one of the most health problems. Almost more than 350 million infected persons were reported universally. Blood transfusion is commonly the most common route of transmission of HBV. Recently, Hospitals in Yemen are increasing demands for blood and blood products due to war injury, anemia, and malnutrition. The risk of transfusion transmission of infection relatively increases. This study aimed to determine hepatitis B virus prevalence among blood donors at the National Blood Transfusion Center -Taiz branch (NBTRC- TB). Data was collected from the National Blood Transfusion and Research Center (Taiz branch) from 1/4/2020 to 16/12/2020. A total of 3174 blood donors donated blood at the center. A descriptive cross-sectional study was conducted on them. Blood donor information was registered at the reception department, and all blood screening tests were performed. Data of HBsAg and total anti-HBc were analyzed statistically by using IBM SPSS version 26. Among 3174 blood donors, male blood donors were 3158 (99.5%) and female blood donors 16 (0.5%). Furthermore, 41 (1.3%) were positive for HBsAg (which all the positive results were for male donors and no positivity were for female donors) while 353 (11.1%) were positive for total anti- HBc Ab which is distributed at ratio of 11% (350) for males and 0.1% (3) for females. On the other hand, the result of HBsAg and total anti-HBc Ab together showed three levels of positivity as the (HBsAg positive / anti-HBc negative) were 12 (0.4%) in which was a low percentage and reversely, the (HBsAg negative/ HBcAb positive) were 316 (10.2%), While the HBsAg positive / anti-HBc positive were 27 (0.9%). So this study shed light on the result of HBsAg negative/ anti-HBc positive which the percentage (10.2%) of which statistically significant (p. value = 0.000) and was the highest result indicates donors with post HBV infection or have low HBV infection. This study showed the high prevalence of post-HBV infection among blood donors. Using both markers HBsAg and total anti-HBc Ab will improve the detection of HBV before blood transfusion.

Improving Hepatitis B diagnosis by implementing statistical quality controls

Hepatitis B is a viral infection that causes major health problems worldwide. The hepatitis B virus (HBV) and 1.2 million deaths per year globally infect more than two billion people. Hepatitis B mainly affects the liver and causes liver cirrhosis and hypocellularity carcinoma. This study investigates diagnostic quality parameters of quantitative polymerase Chain Reaction (qPCR) and enzyme-linked Immunosorbent Assay (ELISA) called enzyme immunoassay (EIA) for HBV Diagnosis. The research was conducted at the Molecular Biochemistry Laboratory (MBL) in the Department of Biochemistry at the University of Agriculture, Faisalabad, Pakistan. The samples for the randomized study containing 977 male and female samples who had pre-diagnosis HBV infection were selected for this comparative study and collected from the Punjab Institute of Nuclear Medicine (PINUM) Hospital and Allied Hospital Faisalabad, Pakistan. This study compared the sensitivity and specificity of the ELISA assay with the HBV qPCR assay to diagnose HBV infection. The cut-off value &lt; 1.00 was considered non-reactive, whereas ≥ 1.00 was reactive patients for ELISA. Similarly, HBV viral load was measured on qPCR &lt; 101 IU/mL was considered a negative result, and &gt; 101 IU/mL showed positive results. Statistical data analysis was conducted using Statistical Package for Social Sciences (SPSS 22) software. These tests were used to diagnose HBV infection on a large scale to calculate the percentage value of sensitivity, specificity, and other parameters. With a 95% confidence interval, the qPCR's positive predictive value (PPV) was 46%, whereas 52% for ELISA. The negative predictive value (NPV) for qPCR was 98%, but it was the same for ELISA. The specificity for qPCR was 91% and 92% for ELISA. The sensitivity value for qPCR was 83%, and 87% for ELISA was observed from the samples. Accuracy for both methods varied, which showed their proficiency and size. The results obtained from qPCR were more accurate and authentic than those obtained from ELISA.

Insights into Immune Exhaustion in Chronic Hepatitis B: A Review of Checkpoint Receptor Expression.

Hepatitis B, caused by the hepatitis B virus (HBV), often progresses to chronic infection, leading to severe complications, such as cirrhosis, liver failure, and hepatocellular carcinoma. Chronic HBV infection is characterized by a complex interplay between the virus and the host immune system, resulting in immune cell exhaustion, a phenomenon commonly observed in chronic viral infections and cancer. This state of exhaustion involves elevated levels of inhibitory molecules, cells, and cell surface receptors, as opposed to stimulatory counterparts. This review aims to elucidate the expression patterns of various co-inhibitory and co-stimulatory receptors on immune cells isolated from chronic hepatitis B (CHB) patients. By analyzing existing data, the review conducts comparisons between CHB patients and healthy adults, explores the differences between HBV-specific and total T cells in CHB patients, and examines variations between intrahepatic and peripheral immune cells in CHB patients. Understanding the mechanisms underlying immune exhaustion in CHB is crucial for developing novel immunotherapeutic approaches. This detailed analysis sheds light on the immune exhaustion observed in CHB and lays the groundwork for future combined immunotherapy strategies aimed at leveraging checkpoint receptors to restore immune function and improve clinical outcomes.

Hepatitis B Reactivation and Vaccination Effectiveness after Solid Organ Transplantation: A Matched Case-Control Study.

Solid organ transplant (SOT) recipients are at significant risk of hepatitis B (HB) virus (HBV) reactivation (HBVr). Despite the clinical significance of HBVr after solid organ transplantation, data on the risk factors for HBVr and vaccine effectiveness in SOT recipients with resolved HBV infection are limited. This study evaluated the risk factors for HBVr and the seroconversion rates after HBV vaccination in SOT recipients. Patients who had undergone solid organ transplantation and those with a resolved HBV infection were identified. We matched patients who experienced post-transplantation HBVr with those who did not. We also explored the characteristics and seroconversion rates of HBV-vaccinated patients following transplantation. In total, 1299 SOT recipients were identified as having a resolved HBV infection at the time of transplantation. Thirty-nine patients experienced HBVr. Pre-transplant HB surface antibodies (anti-HBs) positivity and allograft rejection within 3 months after transplantation were independently associated with HBVr. Among the 17 HBV-vaccinated patients, 14 (82.4%) received three or fewer vaccine doses, and 13 (76.5%) had seroconversion with positive anti-HBs results. Pre-transplant anti-HBs(-) status and allograft rejection were risk factors for HBVr in SOT recipients with a resolved HBV infection, and HBV vaccination after transplantation resulted in a high rate of anti-HBs seroconversion. HBV vaccination after transplantation should be considered to reduce the HBVr risk.