Control of antiviral defenses through hepatitis C virus disruption of retinoic acid-inducible gene-I signaling.

By Eileen M. Foy, Kui Li, R. Sumpter, Y. Loo, C. L. Johnson, Chunfu Wang, P. M. Fish, Mitsutoshi Yoneyama, T. Fujita, S. Lemon and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

602 citations recorded by the source corpus.

Subfields: Hepatology, Immunology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/6c034f10597a0f05e7feeec09b6766559480136d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Hepatology

1. Shizuo Akira
2. P. Farazi
3. R. DePinho
4. Eileen M. Foy
5. J. Hoofnagle
6. M. Gale

In Immunology

1. Shizuo Akira
2. Taro Kawai
3. O. Takeuchi
4. Satoshi Uematsu
5. R. Medzhitov
6. M. Gale
7. Y. Loo
8. Katherine A. Fitzgerald

In Rheumatology

1. Shizuo Akira

Citations in the corpus

• Hepatocellular carcinoma pathogenesis: from genes to environment (2006, background): “In addition, the NS3 and NS4A HCV proteins use their protease function to cleave and activate components that are integral for signalling the immune respons”
• RNA recognition and signal transduction by RIG‐I‐like receptors (2009, background): “By contrast, the protease activity of HCV NS3 ⁄4A is known to be an inhibitor of RIG-Imediated IRF3 activation (114).”
• Innate immune recognition of viral infection (2006, background): “Another example is the NS3-4A protease of hepatitis C virus, which blocks dsRNA-induced interferon production by interfering with IRF3 phosphorylatio”
• Interferons at age 50: past, current and future impact on biomedicine (2007, background): “For example, a hepatitis C virus (HCv)encoded protease can cleave IPS1 off the mitochondrial membrane and block RIGI/MDA5mediated signalling 20 ”
• 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).”
• The RNA Helicase Lgp2 Inhibits TLR-Independent Sensing of Viral Replication by Retinoic Acid-Inducible Gene-I1 (2005, background): “However, HCV expresses a protease NS3/4A, which ablates NF- B or IRF-3 signaling downstream of RIG-I, thereby attenuating the expression of IFNand host antiviral defense genes that otherwise would suppress HCV replication (39).”
• Mechanism of action of interferon and ribavirin in treatment of hepatitis C (2005, background): “In addition, NS3/4A protease activity ablates HCV-induced signalling of the IFN-β receptor by retinoic-acid-inducible gene I (RIG-I) and, furthermore, HCV protease inhibition restores RIG-I functio”
• Toll-like receptors and innate immunity (2006, background): “NS3-4A counteracts not only TLR3-dependent pathways by targeting Trif for proteolytic cleavage, but also counteracts TLR3-independent pathways by targeting an undefined protein of the RIG-I-dependent pathway [114, 115].”
• Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “, 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.”
• Evasion of intracellular host defence by hepatitis C virus (2005, background): “In vitro studies have shown that this signalling provides an amplification loop to further promote IFN and ISG expression, limiting HCV RNA replicatio”