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Evasion of intracellular host defence by hepatitis C virus

An Erratum to this article was published on 08 September 2005

Abstract

Viral infection of mammalian cells rapidly triggers intracellular signalling events leading to interferon α/β production and a cellular antiviral state. This ‘host response’ is our first line of immune defence against infection as it imposes several barriers to viral replication and spread. Hepatitis C virus (HCV) evades the host response through a complex combination of processes that include signalling interference, effector modulation and continual viral genetic variation. These evasion strategies support persistent infection and the spread of HCV. Defining the molecular mechanisms by which HCV regulates the host response is of crucial importance and may reveal targets for novel therapeutic strategies.

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Figure 1: Molecular processes that signal the host response to HCV infection.
Figure 2: Triggering IRF-3 activation by HCV through RIG-I or TLR3, and signalling control by NS3/4A.
Figure 3: HCV attenuates IFN signalling through multiple mechanisms.
Figure 4: HCV–host interactions regulate the host response and affect the outcome of HCV infection.

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Acknowledgements

We thank S. Lemon and members of our laboratory for discussions and critical evaluation of this manuscript. The Gale laboratory is supported by grants from the NIH, the Ellison Medical Foundation and the Burroughs Wellcome Fund. M.G. is the Nancy C. and Jeffrey A. Marcus Scholar in Medical Research in Honor of Dr Bill S. Vowell.

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Gale, M., Foy, E. Evasion of intracellular host defence by hepatitis C virus. Nature 436, 939–945 (2005). https://doi.org/10.1038/nature04078

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