Zihong Chen

TL;DR: It is concluded that hepatocytes contain two distinct antiviral signaling pathways leading to expression of type I IFNs, one dependent upon TLR3 and the other dependent on RIG-I, with little cross-talk between these pathways.

TL;DR: It is shown here that infection of SARS-CoV triggers a weak IFN response in cultured human lung/bronchial epithelial cells without inducing the phosphorylation of IFN-regulatory factor 3 (IRF-3), a latent cellular transcription factor that is pivotal for type I IFN synthesis.

TL;DR: C cultured tamarin hepatocytes show that GBV-B NS3/4A protease effectively blocks innate intracellular antiviral responses signaled through the RNA helicase, retinoic acid-inducible gene I (RIG-I), an essential sensor molecule that initiates host defenses against many RNA viruses, including HCV.

TL;DR: It is shown here that a cpBVDV (NADL strain) does not induce interferon responses in cell culture and blocks induction of interFERon-stimulated genes by a super-infecting paramyxovirus, suggesting that inhibition ofInterferon production is a shared feature of both ncp andcpBVDVs and provide new insights regarding IRF-3 regulation in pestivirus pathogenesis.

TL;DR: In this paper, the authors identify a short-hairpin RNAs (shRNAs) that potently activates the type I interferon (IFN) pathway in human cells in a sequence-and 5′-triphosphate-dependent manner.