Performance of the ELITe InGenius system for hepatitis B virus DNA quantification.

A woman in her 20s from Vietnam, an asymptomatic hepatitis B virus (HBV) carrier with a high viral load, was initiated on tenofovir disoproxil fumarate (TDF) at 31 weeks of gestation. TDF was discontinued after delivery; however, at eight weeks postpartum, she developed an acute exacerbation of hepatitis, characterized by elevated ALT levels and HBV DNA rebound. Although the risk of hepatitis flares following TDF discontinuation is generally considered low, this case highlights the potential for severe postpartum exacerbation and underscores the importance of considering continued antiviral therapy in the postpartum period.

Chronic hepatitis B virus (HBV) infection remains a significant global health challenge. While the dynamic interplay between viral replication and host immune responses determines infection outcomes, the mechanisms driving the resolution of acute infection versus the emergence of chronicity remain incompletely understood. To address this challenge, we developed a detailed quantitative systems pharmacology (QSP) model of acute HBV infection capturing several key host immune and viral mechanisms absent in previous models. The model was parameterized using publicly available data and calibrated against clinical time-course datasets from multiple acute HBV case studies. Perturbation and local sensitivity analyses identified key drivers of biomarker dynamics, particularly hepatitis B virus DNA (HBV DNA), hepatitis B surface antigen (HBsAg), and alanine aminotransferase (ALT). These dynamics were most sensitive to parameters governing viral replication (e.g., HBV entry via the sodium taurocholate cotransporting polypeptide [NTCP] receptor, covalently closed circular DNA [cccDNA] formation, and hepatocyte turnover) and adaptive immune responses (e.g., CD8+ T cell activity, dendritic cell-mediated priming, and regulatory T cell [Treg]-driven immunosuppression). These influential parameters were used to generate a virtual population that reproduced the observed heterogeneity in biomarker trajectories. Notably, the magnitude and timing of biomarker peaks captured most of the variability, reflecting interindividual differences in individual immune responses and viral dynamics. While the current model nicely captures processes associated with acute HBV infections, it will be extended to different stages of chronic HBV with the objective of informing the rational design of novel therapies and supporting the development of curative HBV strategies.

The onset of COVID-19 and subsequent restrictive measures have impacted various infectious diseases, including hepatitis B virus (HBV). This study explored the epidemiological characteristics of HBV infection in Chinese adults before, during the pandemic, and after the easing of restrictive measures. This population-based cohort study used the data from 23,316 adult patients in the southwest of China who had HBV DNA tests from 1 January 2018 to 31 December 2023. HBV DNA was detected in patient serum using real-time fluorescent quantitative PCR. The positive rate of HBV detection was adjusted by age groups, sex, patient types, and seasons, stratified by the stages of the COVID-19 pandemic. Our analysis revealed significant variations in HBV DNA test positivity rates, primarily influenced by age and the pandemic stages. Positivity rates were highest in the 18-25 age group at 0.50 and decreased with advancing age. Males under 35 were at higher risk. Inpatients had the highest positivity rate at 0.42, with seasonal fluctuations peaking in winter. The pandemic stages significantly affected positivity rates, especially in the 36-45 and 56-65 age groups. The findings highlight a complex interplay between pandemic conditions and observed positivity rates. The increase likely stemmed from multiple factors, including shifted testing focus, altered healthcare-seeking behavior, and potential viral reactivation. The COVID-19 response offers insights for optimizing future viral hepatitis control strategies during public health emergencies. Future research should expand demographic and geographic scope and investigate behavioral/social determinants to elucidate underlying mechanisms and guide targeted interventions.

We aimed to evaluate the efficacy and safety of using/not using the antiviral drug tenofovir disoproxil fumarate (TDF) in preventing mother-to-child transmission (MTCT) of hepatitis B virus (HBV) among pregnant women with high serum HBV DNA viral loads. This retrospective study included 512 pregnant women with HBV infection and a high serum HBV DNA load (> 2 × 105 IU/mL) diagnosed and treated at our hospital between January 2018 and April 2023. Based on the treatment received, 314 women were identified as the TDF-treated group, while the remaining 198 comprised the TDF-unexposed group. All newborns received hepatitis B immune globulin and hepatitis B vaccine immediately after birth. Serum HBV DNA, HBsAg, HBeAg, total cholesterol (TC), and alanine aminotransferase (ALT) levels were compared before treatment and prior to delivery. The HBV infection rates of newborns (HBV DNA, HBsAg, HBeAg positivity), maternal adverse events, cesarean section rates, and pregnancy outcomes were also analyzed. Before delivery, serum HBV DNA, HBsAg, HBeAg, and ALT levels decreased in both groups, with significantly greater reductions in the TDF-treated group (P < 0.05). No significant differences were observed in TC levels, adverse drug reactions, cesarean section rates, or adverse pregnancy outcomes (P > 0.05). the HBV DNA, HBsAg, and HBeAg positivity rates of newborns were significantly lower in the TDF-treated group than those in the TDF-unexposed group (P < 0.05). Neonatal body mass index, 1-min Apgar scores, and adverse neonatal outcomes did not differ significantly between groups (P > 0.05). TDF tablets can prevent MTCT of HBV in pregnant women with high HBV DNA loads. The treatment increases the seroconversion rates of HBV DNA, HBeAg, and HBsAg in mothers and infants, and shows a favorable safety profile without severe adverse outcomes.

Abstract Evidence regarding infants with chronic hepatitis B virus (HBV) infection receiving antiviral therapy remains limited. In this cases report, we describe four infants aged 7–10 months diagnosed with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB). CHB01, CHB03, and CHB04 demonstrated active HBV replication and elevated alanine aminotransferase (ALT) levels. CHB02 presented with a relatively low HBV DNA level (3.52 log 10 IU/mL), a low hepatitis B surface antigen (HBsAg) titer (4 IU/mL), and a normal ALT level. With parental consent, all four infants received Lamivudine (LAM) monotherapy before one year of age. Finally, all achieved undetectable HBV DNA after a mean of 5.5 months, HBeAg seroconversion at 8.5 months, HBsAg loss at 7.0 months, and functional cure at 11 months on average. This suggests that early initiation of antiviral treatment may help achieve functional cure for infants with HBeAg-positive CHB.

Linkage of hepatitis B virus (HBV)-infected individuals to medical care is a major hurdle in the HBV elimination care cascade. This study aimed to investigate the rate and factors influencing specialist referral of HBV cases identified in health check programs. This was a retrospective study among consecutive individuals undergoing health check programs with hepatitis B surface antigen (HBsAg) tested in a hospital from 2014 to 2023. Clinical data were captured from the hospital electronic database. Letter of referral after health check was recorded. A total of 28 940 individuals underwent health check with HBsAg tested. Six hundred and seventy-three HBsAg-positive individuals were eligible for analysis. Overall, 322 (47.8%) individuals received referral to hepatology specialist. There was a trend of increasing referral with time over the 10 years; trend slope (95% confidence interval): 5.0% (3.5%-6.4%) per year; p < 0.001. HBV DNA was tested in 207 (30.8%) individuals. On multivariable analysis, with reference to individuals with no HBV DNA tested, HBV DNA ≥ 2000 IU/mL was the strongest independent factor associated with referral (adjusted odds ratio 21.42; 95% confidence interval 8.79-52.24; p < 0.001). Detectable HBV DNA < 2000 IU/mL had a modest association with referral (adjusted odds ratio 1.84; 95% confidence interval 1.08-3.11; p = 0.024). Elevated HBV DNA is an important factor associated with specialist referral among HBsAg-positive individuals identified at health check programs. These findings suggest that implementing reflex HBV DNA testing could be a key strategy to improve specialist referral and facilitate linkage to care.

Background and Aims:Immunosuppression can cause hepatitis B virus (HBV) reactivation, leading to severe outcomes in patients with “resolved” HBV infection. This multicenter, randomized, placebo-controlled trial assessed the efficacy of preemptive antiviral therapy in HBsAg-negative, anti–HBc-positive patients receiving rituximab-based chemotherapy for non-Hodgkin lymphoma (NHL).Methods:Patients were randomized 1:1 to tenofovir alafenamide (TAF)/placebo across 3 phases: chemotherapy plus TAF/placebo (phase 1), TAF/placebo post-chemotherapy (phase 2), and follow-up after therapy cessation (phase 3). The primary endpoint was HBsAg reverse seroconversion. HBsAg and ALT were monitored every 3–12 weeks, depending on treatment phase, and HBV DNA was measured post hoc. ClinicalTrials.gov (NCT02186574).Results:Among 42 patients (median age 65.2 years, 52.4% male, 52.4% aggressive lymphoma, 73.8% anti-HBs positive), 20 received TAF and 22 received a placebo. Median ALT was 20.0 U/L (IQR: 15.0–28.0) at baseline. Median follow-up was 69.4 weeks (IQR: 63.7–166), with 6.1 weeks (IQR: 4.7–8.3) between visits. During follow-up, 2 patients in the TAF arm, but none receiving placebo, experienced HBsAg reverse seroconversions: occurring in phase 3 at 62.3 weeks from baseline, and in phase 1 at 20.0 weeks from baseline. Neither patient experienced ALT >2× ULN. HBV DNA >1000 IU/mL was observed in 8 instances among 6 patients, 3 in each arm, with no associated hepatitis. Low-level DNA (<1000 IU/mL) was not indicative of reverse seroconversion, DNA increases, or ALT elevations.Conclusions:The use of preemptive TAF therapy did not reduce the risk of HBsAg reverse seroconversion; however, the findings should be interpreted with caution as the study was underpowered due to slow enrolment leading to early termination. Low-level HBV DNA elevations were not associated with HBV reactivation. Thus, close HBsAg and ALT monitoring are adequate in HBsAg-negative patients undergoing rituximab-based chemotherapy.

Despite achieving undetectable hepatitis B virus (HBV) DNA levels with nucleos(t)ide analogue (NA) therapy, patients with chronic hepatitis B (CHB) remain at risk of hepatocellular carcinoma (HCC). Novel covalently closed circular DNA activity biomarkers may improve risk stratification. To comprehensively assess the association between serum HBV RNA and hepatitis B core-related antigen (HBcrAg) levels, measured upon achieving undetectable HBV DNA levels, and subsequent HCC development in NA-treated patients with CHB. We retrospectively analysed 311 patients with CHB who achieved undetectable HBV DNA levels during NA therapy between 2000 and 2024. Serum HBV RNA (≥ 10 copies/mL) and HBcrAg (≥ 2.1 log U/mL) were measured in stored samples collected when HBV DNA first became undetectable. Cox regression analysis was performed to identify the factors associated with HCC development. During a median follow-up of 11.0 years, 31 (10.0%) patients developed HCC. At viral suppression, 132 (42.4%) patients had HBV RNA ≥ 10 copies/mL. HCC incidence was significantly higher in patients with quantifiable HBV RNA than in those with unquantifiable HBV RNA (15-year incidence, 17.8% vs. 8.8%, p = 0.026). Quantifiable HBV RNA independently predicted HCC (adjusted hazard ratio [aHR], 3.313; 95% confidence interval [CI]: 1.154-9.507; p = 0.026). HBcrAg showed no association (aHR, 0.821; 95% CI: 0.253-2.669; p = 0.743). Patients with quantifiable HBV RNA and albumin-bilirubin score ≥ -2.60 had the highest risk (5-year incidence: 15.8%). HBV RNA levels at viral suppression predict HCC development in NA-treated patients with CHB, outperforming HBcrAg. Incorporating HBV RNA assessment can improve risk-stratified HCC surveillance strategies.

More aggressive initiation of antiviral treatment contributes to blocking mother-to-child transmission of HBV DNA & RNA in neonatal umbilical cord blood.

Mechanistic study on HuaganJiedu decoction in treating hepatitis B based on multi-omics analysis of network pharmacology, metabolomics, and transcriptomics.

Current therapeutics for chronic hepatitis B virus (HBV) infection are insufficient due to immune exhaustion caused by high circulating hepatitis B surface antigen (HBsAg) levels. Here, an HBV S region-targeted small interfering RNA (siRNA) is reported, aiming to dramatically suppress HBsAg and provide windows for host immune restoration. This siRNA agent, called KC13-M2G2, exhibits potent antiviral efficacy against all HBV genotypes in vitro. Notably, in multiple mouse models, KC13-M2G2 triggers rapid and sustained loss of HBsAg and HBV DNA accompanied by hepatitis B surface antibody seroconversion, outperforming the clinical drug elebsiran and bepirovirsen. Toxicity studies in Sprague-Dawley rats and cynomolgus monkeys indicate satisfactory biosafety profiles of KC13-M2G2. Given that elebsiran and bepirovirsen have achieved a functional cure rate of no more than 20% in their clinical studies, KC13-M2G2 as a more potent candidate drug is expected to exhibit superior performance in clinical applications.

The diagnostic value of hepatitis B core-related antigen in occult hepatitis B virus infection and its related hepatocellular carcinoma.

BACKGROUNDHepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with hepatitis B virus (HBV) infection serving as a significant etiological factor in endemic regions. Alpha-fetoprotein (AFP), the most commonly used biomarker, has limited sensitivity, particularly in AFP-negative HCC. Recent studies have identified origin recognition complex subunit 1 (ORC1) and extra spindle pole bodies-like 1 (ESPL1) as promising serum biomarkers, both linked to HBV DNA integration, a mechanism known to drive hepatocarcinogenesis.AIMTo assess serum ORC1’s diagnostic value for HBV-HCC and its link to S gene integration.METHODSIn this case-control study, 479 HBV-infected patients were enrolled, including 20 with HBV S gene integration, 47 with non-S gene integration, 162 with chronic hepatitis B, 154 with HBV-related cirrhosis, and 96 with HBV-HCC. The control group comprised 73 individuals: 29 with non-HBV-HCC and 44 healthy participants. Serum ORC1 and ESPL1 were measured by enzyme-linked immunosorbent assay. HBV integration sites were identified via whole-genome sequencing. Diagnostic performance was assessed using receiver operating characteristic analysis, including in AFP-negative patients.RESULTSHBV integration near the ORC1 locus (chromosome 1p32.3) was detected in 71.4% of HBV-HCC tissues. Serum ORC1 levels were significantly higher in HBV-infected patients than in non-HBV-infected controls (980.11 ng/L vs 746.82 ng/L, P < 0.05) and in HBV-HCC compared with non-HBV-HCC (1077.07 ng/L vs 749.54 ng/L, P < 0.05). Serum ORC1 and ESPL1 were elevated in HBV-HCC regardless of AFP status, and detected 64.8% and 73.2% of AFP-negative cases, respectively. The combined panel of ORC1 [Area under receiver operating characteristic curve (AUC) = 0.587], ESPL1 (AUC = 0.776), and AFP (AUC = 0.844) achieved an AUC of 0.887, significantly higher than any single marker (P < 0.05), with a sensitivity of 84.44%, specificity of 84.19%, and a negative predictive value of 94.91%.CONCLUSIONSerum ORC1, driven by HBV integration, is a promising biomarker especially for AFP-negative HBV-HCC. Its combination with ESPL1 and AFP significantly improves early detection.

Serological and molecular screening for Hepatitis B virus (HBV) has been essential in reducing the risk of transfusion-transmitted infection, particularly in regions of high endemicity. This retrospective study aimed to analyze the epidemiological profile and laboratory outcomes of 259 blood donors deemed ineligible after initial reactive or inconclusive screening for HBV markers. Donors were summoned for revaluation at the HEMOPA Foundation, in Belém, Pará, between February 2015 and July 2016. Demographic data, risk factors, and results for HBsAg, anti-HBc, anti-HBs, and HBV DNA obtained at the donation and return time points were collected. The mean age was 37 ± 11.25 years, with a predominance of males (56.8%) and first-time donors (76%). At the return time point, 63.7% presented a profile indicative of resolved HBV infection and 3.5% of active infection, 6.6% were susceptible to HBV infection, and 1.9% presented vaccine-induced HBV immunity. Cases of Occult Hepatitis B Infection (OBI, 0.4%) and Window Period (WP, 0.4%) were also identified. The findings reveal a high prevalence of resolved HBV infection among ineligible donors, particularly first-time donors, and reinforce the importance of combined serological and molecular screening, as well as the need for vaccination and health education strategies for at-risk populations. As a public blood bank located in the Amazon region, we highlight that local epidemiological specificities must be considered in the formulation of public health policies that are sensitive to the regional context.

Nucleos(t)ide analogue (NUC) cessation can induce a functional cure in chronic hepatitis B virus (HBV) infections, but severe post-cessation virologic relapses (SVRel) and severe biochemical flares (SBF) frequently occur. To identify predictive biomarkers for patients at highest risk for SVRel and SBF. In the multicentre prospective COIN-B trial, start-of-treatment HBeAg-negative, long-term virologically suppressed patients without advanced fibrosis are followed up for 72 weeks after NUC cessation. We performed a predefined exploratory analysis of the associations between HBV genotype, or end-of-treatment (EOT) biomarkers (HBcrAg, HBV RNA, HBsAg, and anti-HBc IgG) and SVRel (HBV DNA > 5 log IU/mL) or SBF (ALT > 10× ULN) within 48 weeks post-cessation. Of 91 recruited patients, 85 completed 48 weeks of follow-up. SVRel and SBF occurred in 36 (42.4%) and 21 (24.7%) patients, respectively. Genotypes C, D, and E were associated with higher relapse and flare rates, whereas none of the 18 genotype A patients developed SBF. In multivariate analysis, SVRel was independently associated with detectable HBcrAg (aOR 3.93, p = 0.01), and SBF with non-A genotype (aOR 19.03, p = 0.018), detectable HBV RNA (aOR 7.84, p = 0.005), and lower anti-HBc IgG levels (aOR 0.31, p = 0.016). A risk stratification tool, the COBRA score, was developed incorporating HBcrAg, HBV RNA, and anti-HBc IgG. A score ≥ 2 identified patients at increased risk, with 80.0% sensitivity and 90.7% NPV for SBF. HBV genotype and EOT biomarkers, including HBcrAg, HBV RNA, and anti-HBc IgG predict SVRel and SBF following NUC cessation. The COBRA score enables pragmatic, individualised risk stratification. ClinicalTrials.gov identifier: NCT04779970, EudraCT: 2021-001003-32.

Treatment of hepatitis B virus (HBV) infection reduces the risk of disease progression and negative outcomes such as hepatic decompensation and hepatocellular carcinoma (HCC). Studies from select populations in the US suggest that treatment levels are low; whether this pattern occurs nationally remains unclear. To identify HBV treatment levels among patients who met American Association for the Study of Liver Diseases 2016 and 2018 qualification criteria in a clinical setting. This cross-sectional study included adult patients (aged ≥18 years at index) with an HBV diagnosis in the TriNetX Dataworks-USA Network from April 1, 2016, to December 31, 2022, with an HBV DNA laboratory result (index date), measurement of alanine aminotransferase level (2 months before to 1 month after the index date), database encounter activity (6 months or more before the index date), and no evidence of HIV, hepatitis C or D virus infection, HCC, or liver transplant. Data were analyzed from April 1, 2016, to December 31, 2022. International Statistical Classification of Disease, Tenth Revision, codes for HBV diagnosis, procedures, assessments, and dispensing of medication and demographic and laboratory data. Treatment was defined by receipt of a prescription for an anti-HBV agent identified in the data with RxNorm codes. Among 14 693 patients with HBV, 8594 met inclusion criteria, and 2134 were treated. Median age (overall, 46 [IQR, 36-57] years) was similar among treated and untreated individuals (49 [IQR, 38-61] and 45 [IQR, 35-56] years, respectively). While 4423 patients (51.5%) were female, only 538 (12.2%) qualified for treatment, compared with 904 of 4171 male patients (21.7%). Only 414 of the 724 patients (57.2%) who qualified via elevated biochemical and viral levels received treatment. Among 723 patients with advanced fibrosis (Fibrosis-4 score > 3.25) and 587 with diagnosed cirrhosis or liver decompensation, 313 (43.3%) and 235 (40.0%), respectively, were untreated. In multivariable analysis among the overall cohort, female patients were 33.0% less likely to be treated than male patients (odds ratio [OR], 0.67; 95% CI, 0.60-0.75). Compared with Asian patients, lower treatment odds were observed for African American or Black patients (OR, 0.66; 95% CI, 0.58-0.75) and White patients (OR, 0.80; 95% CI, 0.69-0.93) and those of unknown or other race (OR, 0.72; 95% CI, 0.61-0.84). In this cross-sectional study of patients with HBV infection in the US, substantial proportions of patients who met treatment criteria, including those with advanced disease, were untreated, with differences by sex and race. These findings highlight missed opportunities for prevention of negative HBV-related outcomes.

Despite effective antiretroviral use, the incidence of hepatocellular carcinoma (HCC) has not decreased in human immunodeficiency virus (HIV) and hepatitis B virus (HBV) coinfection. Our study compared postoperative prognosis, HBV Pre-S deletion, and immune microenvironment in coinfected and HBV-mono-infected individuals. This retrospective study included 143 HBV-associated HCC patients who underwent curative resection. Virologically suppressed patients (HBV DNA < 1000 IU/mL and HIV RNA < 20 copies/mL) were matched by 1:3 propensity score matching (PSM). Hepatitis B virus Pre-S region was amplified by nested polymerase chain reaction (PCR) and sequenced. Tumor-infiltrating lymphocytes (CD3, CD4, CD8) were quantified by immunohistochemistry. Survival outcomes (recurrence-free survival [RFS] and overall survival [OS]) were analyzed using Kaplan-Meier curves. Baseline analysis showed higher rates of microvascular invasion (76.9% vs 40.0%, P = 0.010) and capsular invasion (30.8% vs 8.5%, P = 0.043) in the HIV/HBV-HCC group. After PSM, compared with HBV-HCC, HIV/HBV-HCC had a higher rate of RFS (hazard ratio [HR] = 4.03, 95% CI 0.96-16.81; P = 0.0058) and OS (HR = 12.04, 95% CI 2.24-64.65; P < 0.0001) was significantly worse. The HIV/HBV-HCC liver tissues showed an increased frequency of Pre-S quasispecies deletion (p = 0.003) and decreased intrahepatic CD4+ infiltration (tumor: P = 0.01; adjacent: P = 0.007). CD8+ expression was lower in coinfected tumors than in HBV-mono-infected tumors (P = 0.039). Virus-suppressed HIV/HBV-HCC showed a worse prognosis, with more Pre-S deletion mutants and more severe T-cell depletion observed in the liver, requiring further investigation of the mechanism.

BackgroundPrecore/Basal core promotor (PC/BCP) mutations are critical mechanisms by which hepatitis B virus (HBV) evades host immunity and antiviral therapy. These mutations are prevalent in HBeAg-positive chronic hepatitis B (CHB) patients, potentially leading to suboptimal responses to nucleos(t)ide analogues (NAs) and high relapse risk after treatment discontinuation.ObjectiveThis study aimed to investigate the impact of PC/BCP mutations on seroconversion and relapse rates and analyze their association with drug resistance mechanisms. The study also evaluated the significance of mutation count (one, two, or three mutations) and specific types of mutations (A1762T, G1764A, G1896A) in relation to the seroconversion and relapse processes.MethodsFrom 2016 to 2019, 48 HBeAg-positive CHB patients were collected and divided into mutation (n=37) and non-mutation (n=11) groups based on PC/BCP status. Seroconversion rates after 144 weeks of NA therapy and relapse rates after 48 weeks of treatment discontinuation were analyzed. Baseline viral load (HBV DNA), liver function (ALT), and Precore/ Basal Core Promoter (PC/BCP) mutation status were analyzed for their correlation with clinical outcomes.ResultsAmong the 37 patients in the mutation group, 9 exhibited G1896A mutation, 15 exhibited A1762T/G1764A double mutations, 13 exhibited A1762T/G1764A/G1896A triple mutations. The mutation group showed significantly lower seroconversion rates than the non-mutation group (37.8% vs 81.8%, P=0.016). The seroconversion rate was inversely correlated with the number of mutations, with triple mutations (A1762T, G1764A, G1896A) associated with the lowest seroconversion rate. The mutation group exhibited a 100% relapse rate (14/14 cases) with HBeAg reactivation, while no relapses occurred in the non-mutation group (0/9 cases, P=0.0001). PC/BCP mutations (eg, A1762T/G1764A) likely reduce NA sensitivity by enhancing viral replication (upregulating pgRNA transcription) and immune evasion (HBeAg epitope variation), leading to delayed treatment response and viral rebound after discontinuation of therapy.ConclusionPC/BCP mutations are independent risk factors for poor NA response and high relapse rates in HBeAg-positive CHB patients. Patients with these mutations should be managed as “occult HBeAg-negative CHB” to avoid premature treatment discontinuation. Routine PC/BCP mutation testing is recommended to guide individualized treatment duration in HBeAg-positive CHB patients.

Introduction: Chronic hepatitis B virus (HBV) and C Virus (HCV) infection are important cause of cirrhosis of liver and Hepatocellular carcinoma (H.C.C). Majority of patients are asymptomatic and are detected incidentally before surgery, pregnancy, blood donation, dialysis and thalassemia treatment. Aims and Objectives: To determine prevalence of HBV &amp; HCV among blood donors and dialysis patients. Materials &amp; Methods: It was prospective study conducted at Department of Medical Gastroenterology, Post Graduate Institute of Medical Sciences (PGIMS), Rohtak, over a period of one year from 1st April, 2024 to 31st March, 2025 during which 40266 blood donors and 17474 dialysis patients were screened for HBV and HCV infections by HbsAg and anti HCV antibody test who were further confirmed by HBV DNA Quantitative and HCV RNA Quantitative test and treated as per scientific protocol. Results: Out of the 40266 blood donors, 354 (0.88%) were HBV positive and 476 (1.18%) were HCV positive. On analysis of 17,474 dialysis patients, 130 (0.88%) were HBV positive and 476 (1.18%) were HCV positive. Conclusion: In view of asymptomatic nature in majority of HBV and HCV patients, manoeuvres to detect at early stage should be taken on broader front. The awareness regarding blood donation is one of them, as it is beneficial for both donor and recipient. The patients on dialysis are also at risk of getting these infections, hence are screened regularly for the same, so that extra care regarding strict infection control practices can be taken to reduce transmission to other patients. Key words: Hepatitis C virus, Hepatitis B virus, Blood Donation, Dialysis, HCV RNA Quantitative test; Anti HCV antibody, HbsAg, HBV DNA Quantitative