Regulating Intracellular Antiviral Defense and Permissiveness to Hepatitis C Virus RNA Replication through a Cellular RNA Helicase, RIG-I
By R. Sumpter, Y. Loo, Eileen M. Foy, Kui Li, Mitsutoshi Yoneyama, T. Fujita, S. Lemon, M. Gale. Journal of Virology, 2005
951 citations recorded by the source corpus.
Subfields: Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/2ea2333c9d0fda890f4544016ff5d5878d0ea929
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Shizuo Akira
- Taro Kawai
- O. Takeuchi
- Himanshu Kumar
- Zhijian J. Chen
- T. Mogensen
- Lijun Sun
- Satoshi Uematsu
Citations in the corpus
- Pattern recognition receptors and inflammation. (2010, background): “In addition to JEV, another flavivirus, hepatitis C virus (HCV), is also recognized by RIG-I, whereas both RIG-I and MDA5 redundantly recognize Dengue virus and West Nile virus (Loo et al., 2008; Sumpter et al., 2005).”
- IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction (2005, background): “For example, human RIG-I has been linked to hepatitis C virus RNA–induced IRF3 activatio”
- 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.”
- MDA5/RIG-I and virus recognition. (2008, background): “However, Dengue virus and West Nile virus, which also belong to the Flaviviridae family, were reported to induce type I IFN production even in the absence of either RIG-I or MDA5 [9 ,14–16].”
- Immune signaling by RIG-I-like receptors (2011, background): “…characterized as a dsRNA-binding protein that triggered IFN induction and virus signaling in response to the synthetic dsRNA poly(I:C) (Yoneyama et al., 2004) and was then identified as a major factor controlling cell permissiveness for hepatitis C virus replication (Sumpter et al., 2005).”
- Mechanism of action of interferon and ribavirin in treatment of hepatitis C (2005, methodology): “In the replicon system, HCV RNA replication has minimal effects on the expression of ISGs, probably because of defects in IFN signalling in the cell lines that support HCV replicon”
- RIG-I uses an ATPase-powered translocation-throttling mechanism for kinetic proofreading of RNAs and oligomerization (2018, background): “The innate immune receptor RIG-I (Retinoic acid Inducible Gene I) recognizes viral RNAs in the cytoplasm and initiates a signaling pathway that creates an antiviral state with the production of interferons and inflammatory cytokines (Poeck et al., 2010; Sumpter et al., 2005; Yoneyama et al., 2004).”
- Flaviviridae :T he Viruses and Their Replication (2007, background): “This is important, because RIG-I activation has been shown to inhibit HCV replication (684), and a dominant negative mutation in RIG-I renders an Huh-7 subline highly permissive for HCV RNA replication (61,684).”