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Sci Rep. 2015 Mar 11;5:9012. doi: 10.1038/srep09012.

Interferon-α inducible protein 6 impairs EGFR activation by CD81 and inhibits hepatitis C virus infection.

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Department of Internal Medicine, Saint Louis University.
Department of Medicinal Chemistry, College of Pharmacy, University of Utah.
1] Department of Medicine and Genetics, University of Arkansas for Medical Sciences [2] The Central Arkansas Veterans Healthcare System.
1] Department of Internal Medicine, Saint Louis University [2] Department of Pathology, Saint Louis University.
1] Department of Internal Medicine, Saint Louis University [2] Department of Molecular Microbiology &Immunology, Saint Louis University.


Viral entry requires co-operative interactions of several host cell factors. Interferon (IFN) and the IFN-stimulated genes (ISGs) play a central role in antiviral responses against hepatitis C virus (HCV) infection. We examined the effect of interferon-α inducible protein 6 (IFI6) against HCV infection in human hepatoma cells. HCV RNA level or infectious foci were inhibited significantly by ectopic expression of IFI6. IFI6 impaired CD81 co-localization with claudin-1 (CLDN1) upon HCV infection or CD81 cross-linking by specific antibody. Activation of epidermal growth factor receptor (EGFR), a co-factor involved in CD81/CLDN1 interactions, was reduced in IFI6 expressing cells in response to HCV infection or CD81 cross linking by antibody, but not by treatment with EGF. Taken together, the results from our study support a model where IFI6 inhibits HCV entry by impairing EGFR mediated CD81/CLDN1 interactions. This may be relevant to other virus entry processes employing EGFR.

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