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DTP-HBV-Hib vaccine (Comvac5)

✓ Approved

Bharat Biotech Ltd. · 疫苗 · 疫苗

什么是 DTP-HBV-Hib vaccine？

DTP-HBV-Hib vaccine 是一种疫苗，由Bharat Biotech Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名Comvac5
公司Bharat Biotech Ltd.
药物类别疫苗
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Bharat Biotech Ltd.

治疗适应症

DTP-HBV-Hib vaccine 针对 4 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsDiphtheria✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsPertussis✓ Approved
Infections and infestationsTetanus✓ Approved

相关研究文献

PubMedViruses2026-10-27

Prevalence and Genetic Diversity of Hepatitis B and C Viruses in People Living with HIV in the Capital District of Venezuela.

Beltrán Julie Andreina JA, Sulbarán Yoneira Fabiola YF, Martínez-Urbina Nahir N, Comegna Mario M et al.

Coinfection between hepatitis viruses and human immunodeficiency virus (HIV) significantly increases liver disease and AIDS progression. This retrospective cross-sectional study evaluated the prevalence and genetic diversity of hepatitis B (HBV) and C viruses (HCV) among people living with HIV (PLWH) in Venezuela's Capital District. A total of 420 serum samples collected between 2022 and 2025 were tested for serological and molecular markers, including whole-genome HBV sequencing via next-generation sequencing (NGS) to characterize viral genotype distribution and mutations. Seroprevalences for HBsAg, anti-HBc, and anti-HCV were 2.9%, 20%, and 4.0%, respectively. HBV exposure was significantly higher in older men, with no differences between treatment-naïve and treated patients. Occult HBV infection (OBI) prevalence decreased compared to 2014 data (seropositive: 7% vs. 16%, seronegative: 0.9% vs. 20%). This decline, along with the higher HBV exposure among older adults, may be partially attributed to the universal HBV vaccination introduced in Venezuela in 1998, as well as modifications in antiretroviral therapy affecting HBV replication. Notably, key vaccine- and diagnostic-escape mutations were detected in OBI cases, highlighting clinical and public health concerns. Increased HCV prevalence appears to be linked to rising intravenous drug use in the country. HBV phylogenetic analysis revealed genotype F3 as predominant, followed by F1b (Cosmopolitan clade), while HCV showed genotype 1a to be the most frequent, followed by 1b and 3a. These findings underscore the success of immunization efforts but highlight the urgent need for continuous molecular surveillance and updated public health policies, including targeted harm-reduction programs, to control viral hepatitis in vulnerable populations.

PMID 42944024
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PubMedViruses2026-10-27

Double-Edged Sword: HBV-Driven Lipid Metabolism Remodeling in Hepatocarcinogenesis Through Ferroptosis Regulation.

Xia Sihan S, Shen Xueqin X, Chen Guangyu G, Liu Ruifang R et al.

Chronic hepatitis B virus (HBV) infection remains a leading cause of hepatocellular carcinoma (HCC) worldwide, particularly in Asia. Although nucleos(t)ide analogs suppress viral replication and reduce HCC incidence, residual risk persists, highlighting the need to better understand HBV-driven hepatocarcinogenesis. HBV alters host transcription, DNA repair, lipid metabolism, and the hepatic immune microenvironment. These changes help sustain liver injury, fibrogenesis, and malignant transformation. Ferroptosis, an iron-dependent form of programmed cell death driven by excessive lipid peroxidation, has emerged as an important mechanism in this context, because the liver is central to iron and lipid metabolism. Here, we propose that HBV-driven lipid remodeling shapes ferroptosis susceptibility in a stage-dependent, double-edged manner. During chronic infection, oxidative stress and enrichment of peroxidation-prone lipid substrates may promote ferroptosis-associated hepatocyte injury, immune dysregulation, and fibrosis. After malignant transformation, HBV-related oncogenic programs may instead favor ferroptosis evasion through altered lipid composition and strengthened antioxidant defenses, thereby supporting tumor survival and progression. In this review, we summarize mechanisms linking HBV, lipid metabolic remodeling, and ferroptosis while distinguishing direct HBV-related evidence from findings inferred from other liver disease or cancer models. This HBV-ferroptosis framework may help refine risk stratification and suggest new therapeutic opportunities in HBV-related HCC.

PMID 42943995
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PubMedMicroorganisms2026-10-27

SLC27A5 Inhibits HBV Replication Through Regulating FXR/SREBP1C/FASN/ACC1 Pathway in HepAD38 Cells.

Cun Mengren M, Liu Yongxin Y, Ma Xinrong X, Zhang Xinran X et al.

Hepatitis B virus (HBV) infection can lead to hepatitis B, which may eventually progress to cirrhosis or hepatocellular carcinoma (HCC). Host lipid metabolism plays a critical role in HBV replication, and HBV infection also impairs lipid homeostasis. The solute carrier family 27 member 5 (SLC27A5) gene, which encodes a long-chain fatty acid transporter and bile acid-CoA ligase, has been reported to be associated with cirrhosis and HCC. However, whether SLC27A5 influences HBV infection or replication remains unclear. In this study, the SLC27A5 gene was overexpressed or silenced in HepAD38 cells. Results show that SLC27A5 overexpressing suppresses HBV replication. Given the primary role of SLC27A5 in bile acid metabolism, we hypothesized that SLC27A5 might inhibit HBV replication via regulating the FXR/SREBP1C/FASN/ACC1 signaling pathway. Subsequent experiments confirmed that overexpression of SLC27A5 upregulated FXR expression levels and downregulated mRNA levels of the SREBP1C, FASN, and ACC1 genes. Consequently, lipid synthesis was suppressed in SLC27A5-overexpressing cells, with significantly reduced levels of lipid droplets and triglycerides. Furthermore, SLC27A5 might collaborate with Entecavir to inhibit HBV replication. In summary, we demonstrated that SLC27A5 inhibited HBV replication through regulating FXR/SREBP1C/FASN/ACC1 and decreasing lipid synthesis.

PMID 42943532
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PubMedMetabolites2026-10-27

Metabolic and Thyroid Alterations in HBV Monoinfection and HBV-HDV Coinfection: Insights from a Liver Transplant Cohort.

Serin Ayfer A, Koçulu Demir Safiye S, Bozkurt Birkan B, Anılır Ender E et al.

Metabolic alterations associated with hepatitis B virus (HBV)-hepatitis D virus (HDV) coinfection remain poorly characterized. We investigated metabolic and endocrine profiles in HBV monoinfection and HBV-HDV coinfection, with emphasis on quantitative HDV activity. This retrospective observational study included HBsAg-positive adult liver transplant candidates. Pre-transplant metabolic, biochemical, thyroid, and virological parameters were evaluated. Associations between quantitative HDV RNA and metabolic parameters were assessed using Spearman correlation and multivariable regression. Conventional circulating metabolic parameters were broadly comparable between groups. HBV-HDV coinfection was associated with higher adjusted odds of diabetes mellitus, although this association was attenuated after accounting for liver disease severity. TSH was independently lower in HBV-HDV coinfection, whereas FT3 and FT4 did not differ independently. Among patients with HBV-HDV coinfection, HDV RNA correlated positively with triglycerides (ρ = 0.437, p = 0.009). Each 1-log10 increase in HDV RNA was associated with a 5.42 mg/dL increase in triglycerides after adjustment for HBV DNA, age, sex, and MELD score (95% CI 1.84-9.00; p = 0.003), with consistent associations in BMI- and diabetes-adjusted sensitivity models. Higher quantitative HDV RNA was independently associated with higher triglyceride concentrations, identifying a potential viral-metabolic interaction that warrants prospective validation.

PMID 42941185
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PubMedFrontiers in microbiology2026-10-27

Metabolic-epigenetic regulation of the HBV cccDNA reservoir: pathways underpinning viral persistence.

Peng Qing Q, Hao Liyuan L, Li Shenghao S, Yu Fei F et al.

Chronic hepatitis B virus (HBV) infection remains a global public health burden, and functional cure represents the primary goal of clinical management. The nuclear covalently closed circular DNA (cccDNA) minichromosome stably maintained in infected hepatocytes constitutes the major barrier to HBV cure. Clinically, functional cure is defined as sustained hepatitis B surface antigen (HBsAg) seroclearance with undetectable serum HBV DNA after finite treatment, a definition that does not require complete cccDNA elimination. At the molecular level, functional cure is thought to be associated with stable transcriptional silencing of cccDNA and integrated HBV DNA, a state biologically distinct from physical cccDNA depletion. Accumulating data demonstrate that the persistence and transcriptional homeostasis of the cccDNA reservoir are controlled by viral proteins and dynamically shaped by host metabolic signaling and epigenetic remodeling. Here, we first outline key steps of the HBV life cycle to establish the mechanistic context for cccDNA formation and replenishment, and then focus our synthesis on the integrated host metabolic-epigenetic network that governs cccDNA establishment, transcriptional activity, stability, and clearance. We dissect how central carbon metabolites, bile acid signaling, histone post-translational modifications, and immune cytokines converge to modulate cccDNA reservoir homeostasis, and critically evaluate the strength of evidence supporting their physiological relevance in the chronically infected human liver. We also discuss mechanisms of HBV immune evasion, including hepatitis B virus X protein (HBx)-driven epigenetic reprogramming and subviral particle-associated immune tolerance. We summarize preclinical and clinical therapeutic strategies targeting the metabolic-epigenetic microenvironment, viral assembly, antigen secretion, and cccDNA modulation to achieve a functional cure for HBV infection. Finally, we outline key unresolved challenges in the field, including the undefined in vivo cccDNA turnover kinetics, the poorly characterized physiological relevance of cell-to-cell transmission, the inherent limitations of gene-editing technologies, and the urgent need for specific non-invasive biomarkers reflecting intrahepatic cccDNA activity.

PMID 42936208
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PubMedCancers2026-10-27

Association of HBsAg Positivity and HBV Reactivation in EGFR-Mutant Lung Adenocarcinoma Treated with EGFR-TKIs: A Retrospective Cohort Study.

Sun Jiayi J, Lin Jingwen J, Li Honglin H, Li Weimin W et al.

EGFR-TKIs serve as standard first-line targeted therapy for EGFR-mutant lung adenocarcinoma (LUAD). Real-world data on the prognostic role of baseline HBsAg positivity and the risk of HBV reactivation during EGFR-TKI treatment remain limited, particularly in HBV-endemic Chinese populations. This retrospective single-center cohort study enrolled 580 consecutive patients with stage III-IV EGFR-mutant LUAD who received EGFR-TKIs between 2013 and 2026. Patients were grouped by baseline HBsAg status; Kaplan-Meier curves and multivariable Cox models adjusted for key clinical covariates were used to evaluate progression-free survival (PFS) and overall survival (OS). HBV reactivation was defined by EASL criteria, with virological evaluation available for 51 of 82 HBsAg-positive patients. Among all enrolled patients, 14.1% were HBsAg-positive. The HBV reactivation rate was 9.8% among evaluable HBsAg-positive patients, and reactivation was not independently linked to survival. After adjustment, baseline HBsAg positivity showed a borderline trend toward poorer OS (HR = 1.42, 95% CI, 0.99-2.04, p = 0.054) without significant PFS association (HR = 1.14, 95% CI, 0.80-1.62, p = 0.481). Liver metastasis independently predicted worse OS in HBsAg-positive patients (HR = 3.84, 95% CI, 1.65-8.94, p = 0.002). HBV reactivation was uncommon but warrants close monitoring during EGFR-TKI therapy. Baseline HBsAg positivity demonstrated only a non-significant trend toward inferior OS without affecting PFS. Routine HBsAg screening at diagnosis may facilitate risk stratification, and HBsAg-positive patients with liver metastasis require intensified surveillance.

PMID 42938905
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