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Objectives: The virological profiles of hepatitis B and C viruses (HBV and HCV) and their interplay in cases of coinfection are undefined. A suppressed and occult HBV infection may occur in hepatitis B surface antigen (HBsAg) negative patients with chronic hepatitis C. The HCV core protein is able to inhibit HBV "in vitro," and serines at positions 99 and 116 are essential for such inhibition. We aimed to assess the HBV and HCV virological profiles in cases of coinfection and to evaluate the relationship between HCV core gene variability and HBV activity.
Methods: Eighty-two anti-HCV positive patients were examined: 35 cases were HBsAg positive, 24 were HBsAg negative with "occult" HBV infection, and 23 were HBV negative. HBV and HCV viremia levels were evaluated in all cases. HCV genomic region coding for the aminoacid sequence 99-116 of core protein was amplified and sequenced in all HCV RNA positive cases. The entire core gene was amplified and sequenced in three randomly selected cases.
Results: Serum HCV RNA was detected in all cases but 13, all HBsAg positive individuals; HCV viremia levels of the other 22 HBsAg positive subjects were similar to those detected in HBsAg negative patients with or without occult HBV infection. Among the 35 HBsAg positive patients both HBV DNA and HCV RNA were detected in five cases, HCV RNA alone in 17, and HBV DNA alone in six, whereas seven cases had undetectable levels of both viruses. Sequencing analyses showed that the HCV core gene was highly preserved in all patients.
Conclusion: A wide spectrum of HCV and HBV virological patterns may occur in a case of coinfection. HCV core variability is not related to HBV activity "in vivo."
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http://dx.doi.org/10.1111/j.1572-0241.2002.05707.x | DOI Listing |
J Virol
September 2025
Department of Hepatology, Center of Infectious Diseases and Pathogen Biology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
Unlabelled: Cholesterol 25-hydroxylase (CH25H), an interferon-stimulated gene (ISG), has been implicated in broad-spectrum antiviral immunity. Here, we identify CH25H as a potent suppressor of hepatitis B virus (HBV) replication that significantly outperforms IFN-α in reducing HBV DNA, pregenomic RNA (pgRNA), HBsAg, and HBeAg, without inducing cytotoxicity. However, CH25H is weakly expressed in hepatocytes and only modestly induced by type I interferon.
View Article and Find Full Text PDFPediatr Infect Dis J
September 2025
From the Pediatric Infectious Diseases Unit, Gregorio Marañón University Hospital, Madrid, Spain.
Background: Vaccination is a key strategy to reduce infectious disease mortality. In pediatric heart transplant recipients (HTRs), the use of immunosuppressive therapy weakens immune responses, increasing the risk of viral infections. This study aimed to evaluate the immunogenicity of hepatitis B virus (HBV) revaccination in this vulnerable population.
View Article and Find Full Text PDFJHEP Rep
October 2025
HEOR-Global Value and Access, Gilead Sciences, Inc., Foster City, CA, USA.
Background & Aims: HDV leads to the most severe form of viral hepatitis. It has been estimated to affect 5-13% of people who have chronic HBV worldwide. Evidence of HDV incidence, prevalence, and disease burden in Spain is limited.
View Article and Find Full Text PDFJ Immunol
September 2025
Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Qidong-Fudan Innovative Institution of Medical Sciences, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large quantities of subviral particles containing its surface antigen (HBsAg). T cells play a central role in controlling HBV infection but can also mediate liver injury and contribute to disease progression. However, the mechanisms that regulate T-cell responses to eliminate the virus without causing immunopathology during acute HBV infection remain poorly defined.
View Article and Find Full Text PDFMol Pharmacol
August 2025
Institute of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Biomedical Research Center Seltersberg, Justus Liebig University of Giessen, Giessen, Germany. Electronic address:
The myristoylated preS1 domain (myr-preS1) of the hepatitis B virus (HBV) large surface protein is essential for binding to the receptor protein, Na/taurocholate co-transporting polypeptide (NTCP), and for the subsequent internalization of the virus-receptor complex. NTCP, which is expressed in hepatocytes, plays a physiological role in hepatic bile acid transport. Recent cryo-electron microscopy structures of the myr-preS1-NTCP complex were used to analyze virus-receptor interactions at the molecular level.
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