Immune evasion by hepatitis C virus NS3/4A protease-mediated cleavage of the Toll-like receptor 3 adaptor protein TRIF.

By Kui Li, Eileen M. Foy, J. Ferreon, Mitsuyasu Nakamura, A. C. Ferreon, M. Ikeda, S. Ray, M. Gale, S. Lemon. Proceedings of the National Academy of Sciences of the United States of America, 2005

1,177 citations recorded by the source corpus.

Subfields: Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/7460abaf706561153ba03cdb5a0f7ffdf1a42a07

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Citations in the corpus

Pathogen recognition and innate immunity. (2006, positive): “Hepatitis C virus (HCV) encodes NS3/4A protease, which blocks IRF-3 activation by cleaving TRIF and thereby subverting poly I:C-mediated activation of IFN responses (Li et al., 2005).”
Evasion of intracellular host defence by hepatitis C virus (2005, background): “The HCV NS3/4A protease functions as an antagonist of virus-induced IRF-3 activation and IFN-β expression through its ability to block RIG-I signalling and to ablate TLR3 signalling by cleaving the TRIF adaptor protei”
Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “…pathways are documented for poxviruses (Harte et al., 2003; DiPerna et al., 2004; Stack et al., 2005) and Hepatitis A & C viruses (Breiman et al., 2005; Fensterl et al., 2005; Foy et al., 2005; Li et al., 2005a, 2005b; Sumpter et al., 2005), but likely many other examples remain to be uncovered.”
Innate immune recognition of viral infection (2006, background): “NS3-4A also mediates TRIF proteolysis, suggesting multiple functions for this proteas”
Interferon signalling network in innate defence (2006, background): “2), which is the critical adaptor protein linking TLR3 to its downstream NF-κB and IRF3 pathways for the double-stranded RNA (ds-RNA) response (Li et al., 2005). ii.”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “endosomal dsRNA (212), NS3/4 also targets IPS-1 and pre-”
Induction of a Striking Systemic Cytokine Cascade prior to Peak Viremia in Acute Human Immunodeficiency Virus Type 1 Infection, in Contrast to More Modest and Delayed Responses in Acute Hepatitis B and C Virus Infections (2009, background): “Additionally, HBV and HCV possess strategies for blocking type I IFN production in the cells which they infect (7, 16, 29, 48).”