期刊
NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
卷 13, 期 10, 页码 580-589出版社
NATURE PORTFOLIO
DOI: 10.1038/nrgastro.2016.126
关键词
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资金
- German Center for Infection Research (DZIF) [TTU 05.901, TTU 05.804, TTU 05.904, TTU 05.704]
- German Research Foundation [UR72/7-1]
- Hartmut Hoffmann-Berling International Graduate School of Molecular and Cellular Biology
Chronic hepatitis D is the most severe form of viral hepatitis, affecting similar to 20 million HBV-infected people worldwide. The causative agent, hepatitis delta virus (HDV), is a unique human pathogen: it is the smallest known virus; it depends on HBV to disseminate its viroid-like RNA; it encodes only one protein (HDAg), which has both structural and regulatory functions; and it replicates using predominantly host proteins. The failure of HBV-specific nucleoside analogues to suppress the HBV helper function, and the limitations of experimental systems to study the HDV life cycle, have impeded the development of HDV-specific drugs. Thus, the only clinical regimen for HDV is IFN alpha, which shows some efficacy but long-term virological responses are rare. Insights into the receptor-mediated entry of HDV, and the observation that HDV assembly requires farnesyltransferase, have enabled novel therapeutic strategies to be developed. Interference with entry, for example through blockade of the HBV-HDV-specific receptor sodium/taurocholate cotransporting polypeptide NTCP by Myrcludex B, and inhibition of assembly by blockade of farnesyltransferase using lonafarnib or nucleic acid polymers such as REP 2139-Ca, have shown promising results in phase II studies. In this Review, we summarize our knowledge of HDV epidemiology, pathogenesis and molecular biology, with a particular emphasis on possible future developments.
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