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Ubiquitinated hepatitis D antigen-induced CD8 T-cell responses inhibit HDV replication in HDV-infected liver organoids.
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Department of Infection, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:
Background: Hepatitis D virus (HDV) infection is the most severe form of human viral hepatitis. A poor virus-specific CD8T cell response may result in persistent HDV infection. We investigated anti-viral effect and mechanisms of ubiquitinated small hepatitis D antigen (Ub-S-HDAg) in HBV/HDV superinfected liver organoids.
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Department of Computer Science, Ben-Gurion University of the Negev, David Ben-Gurion Blvd. 1, Beer-Sheva 8410501, Israel.
Hepatitis delta virus (HDV) is geographically classified according to eight known genotypes. The combined hepatitis B-hepatitis D (HEPB-HEPD) disease is the severest form of chronic viral hepatitis in humans and is characterized by mortality rates of ~20%. Hepatitis delta virus has no FDA approved therapy and its only available vaccine is the one for HEPB.
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Department of Hepatology, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region, China.
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Hepatitis D virus (HDV) infection remains a major cause of severe liver disease among hepatitis B virus (HBV)-infected patients, contributing to accelerated progression to cirrhosis and hepatocellular carcinoma. Pegylated interferon-α remains the first-line therapy for chronic HDV infection in most cases. However, despite its approval for HBV and hepatitis C virus (HCV) infections, its use in HDV is largely driven by a lack of other options and is constrained by its limited efficacy, suboptimal durability of response, and a substantial side effect profile.
View Article and Find Full Text PDFRegulation of viral hepatitis by N6-methyladenosine RNA methylation.
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Division of Infectious Diseases and Global Public Health, Department of Medicine, University of California San Diego, La Jolla, USA.
Recent studies have shown that the presence of an RNA modification, N6-methyladenosine (mA), in viral RNAs during infection significantly impacts the outcome of viral replication and pathogenesis. In particular, various functions of mA have been elucidated in hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV). During viral infection, mA methylation not only directly affects the replication of these viruses but also regulates diverse cellular RNAs to control pathogenesis.
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