Immune evasion by hepatitis C virus NS3/4A protease-mediated cleavage of the Toll-like receptor 3 adaptor protein TRIF
Johns Hopkins University · The University of Texas Southwestern Medical Center
Abstract
Toll-like receptors (TLRs) bind pathogen-specific ligands early in infection, initiating signaling pathways that lead to expression of multiple protective cellular genes. Many viruses have evolved strategies that block the effector mechanisms induced through these signaling pathways, but viral interference with critical proximal receptor interactions has not been described. We show here that the NS3/4A serine protease of hepatitis C virus (HCV), a virus notorious for its ability to establish persistent intrahepatic infection, causes specific proteolysis of Toll-IL-1 receptor domain-containing adaptor inducing IFN-beta (TRIF or TICAM-1), an adaptor protein linking TLR3 to kinases responsible for activating IFN…
Citation impact
- FWCI
- 42.57
- Percentile
- 100%
- References
- 43
Authors
9- KLKui LiCorresponding
Johns Hopkins University, The University of Texas Southwestern Medical Center
- EFEileen Foy
Johns Hopkins University, The University of Texas Southwestern Medical Center
- JCJosephine C. Ferreon
Johns Hopkins University, The University of Texas Southwestern Medical Center
- MNMitsuyasu Nakamura
Johns Hopkins University, The University of Texas Southwestern Medical Center
- ACAllan Chris M. Ferreon
Johns Hopkins University, The University of Texas Southwestern Medical Center
Topics & keywords
- TRIF
- NS3
- Signal transducing adaptor protein
- Biology
- TLR3
- Interferon regulatory factors
- Signal transduction
- Cell biology