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Updated: May 2, 2026

A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Regulation of interferon regulatory factor 3-dependent innate immunity by the HCV NS3/4A protease
1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Abstract:
Interferon regulatory factor 3 (IRF-3) is a ubiquitously expressed latent cellular transcription factor that plays a pivotal role in control of innate, type I interferon (IFN) antiviral responses. After viral infections, IRF-3 is activated by specific C-terminal phosphorylation, which induces its dimerization and nuclear translocation, whereupon IRF-3 activates the transcription of type I IFNs and a number of other antiviral effector genes. Many viruses have evolved strategies that antagonize signaling mechanisms leading to IRF-3 activation. Recent studies have shown that hepatitis C virus blocks IRF-3 activation and subsequent IFN induction by cleaving critical cellular substrates within the intracellular antiviral signaling pathways upstream of IRF-3 with its major protease, NS3/4A.
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