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Hepatitis C virus NS5B polymerase primes innate immune signaling
Institute of Experimental Virology Twincore – Center for Experimental and Clinical Infectious Disease Research Hannover, Germany. (Gisa Gerold)
2013 (English)In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 57, no 3, p. 1275-1277Article in journal (Refereed) Published
Abstract [en]

Innate immunity controls pathogen replication and spread. Yet, certain pathogens, such as Hepatitis C Virus (HCV), escape immune elimination and establish persistent infections that promote chronic inflammation and related diseases. Whereas HCV regulatory proteins that attenuate antiviral responses are known, those that promote inflammation and liver injury remain to be identified. Here, we show that transient expression of HCV RNA-dependent RNA polymerase (RdRp), NS5B, in mouse liver and human hepatocytes results in production of small RNA species that activate innate immune signaling via TBK1-IRF3 and NF-kappa B and induce cytokine production, including type I interferons (IFN) and IL-6. NS5B-expression also results in liver damage.

Place, publisher, year, edition, pages
Hoboken: Wiley-Blackwell, 2013. Vol. 57, no 3, p. 1275-1277
Keywords [en]
de-novo initiation, RIG-I, replication complex, adapter protein, RNA synthesis, infection, pathway
National Category
Gastroenterology and Hepatology
Identifiers
URN: urn:nbn:se:umu:diva-148167DOI: 10.1002/hep.26201ISI: 000315644200047PubMedID: 23426794OAI: oai:DiVA.org:umu-148167DiVA, id: diva2:1210806
Available from: 2018-05-29 Created: 2018-05-29 Last updated: 2018-09-05Bibliographically approved

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