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Robust hepatitis C virus infection in vitro.
TLDR
A simple yet robust HCV cell culture infection system based on the HCV JFH-1 molecular clone and Huh-7-derived cell lines that allows the production of virus that can be efficiently propagated in tissue culture is reported. Expand
Cellular Determinants of Hepatitis C Virus Assembly, Maturation, Degradation, and Secretion
TLDR
The results suggest that by coopting the VLDL assembly, maturation, degradation, and secretory machinery of the cell, HCV acquires its hepatocyte tropism and, by mimicry, its tendency to persist. Expand
Persistent Hepatitis C Virus Infection In Vitro: Coevolution of Virus andHost
TLDR
The establishment and the characteristics of persistent in vitro infection of human hepatoma-derived cells by a recently described HCV genotype 2a infectious molecular clone reveal the existence of coevolutionary events during persistent HCV infection that favor survival of both virus and host. Expand
Identification of a Residue in Hepatitis C Virus E2 Glycoprotein That Determines Scavenger Receptor BI and CD81 Receptor Dependency and Sensitivity to Neutralizing Antibodies
TLDR
Mutation of E2 at position 451 alters the relationship between particle density and infectivity, disrupts coreceptor dependence, and increases virion sensitivity to receptor mimics and NAbs, suggesting the evasion of host immune responses. Expand
Double-stranded DNA and double-stranded RNA induce a common antiviral signaling pathway in human cells
TLDR
Evidence is presented that both retinoic acid-induced gene I (RIG-I) and mitochondrial antiviral signaling protein (MAVS) are required for dsDNA-induced IFN-β promoter activation in a human hepatoma cell line and that activation is efficiently blocked by the hepatitis C virus NS3/4A protease. Expand
Inhibition of dsRNA-induced signaling in hepatitis C virus-infected cells by NS3 protease-dependent and -independent mechanisms.
TLDR
Overexpression of individual components of the dsRNA-signaling pathway in HCV-infected and uninfected cells indicates that HCV inhibits IFN- beta promoter activity by inactivating the mitochondrial antiviral signaling protein/IFN-beta promoter stimulator 1 (MAVS/IPS-1), while leaving the IFn-induced Janus kinases-signal transducers and activators of transcription signaling pathway intact. Expand
IL28B Genetic Variation Is Associated with Spontaneous Clearance of Hepatitis C Virus, Treatment Response, Serum IL-28B Levels in Chinese Population
TLDR
The rs12979860-CC variant upstream of IL28B gene is associated with spontaneous clearance of HCV, susceptible to IFN/RBV treatment and increased IL-28B levels in this Chinese population. Expand
Activation of sterol regulatory element-binding protein 1c and fatty acid synthase transcription by hepatitis C virus non-structural protein 2.
TLDR
The results suggest that HCV NS2 can upregulate the transcription of SREBP-1c and FAS, and thus is probably a contributing factor for HCV-associated steatosis. Expand
Hepatitis C virus NS4B blocks the interaction of STING and TBK1 to evade host innate immunity.
TLDR
A novel NS3/4A-independent mechanism HCV utilizes to evade host innate immune responses in which viral NS4B protein targets STING/MITA to suppress the interferon signaling is reported. Expand
MDA5 plays a critical role in interferon response during hepatitis C virus infection.
TLDR
The data demonstrate that MDA5 recognizes HCV to initiate host innate immune response during HCV infection, providing insight into how host senses HCVs to initiate innate immunity duringHCV infection. Expand
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