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Evidence that hepatitis C virus resistance to interferon is mediated through repression of the PKR protein kinase by the nonstructural 5A protein.
TLDR
It is reported that NS5A represses PKR through a direct interaction with the protein kinase catalytic domain and that both PKR repression and interaction requires the ISDR, suggesting inactivation of PKR may be one mechanism by which HCV avoids the antiviral effects of IFN.
Control of PKR Protein Kinase by Hepatitis C Virus Nonstructural 5A Protein: Molecular Mechanisms of Kinase Regulation
TLDR
Results indicate that mutations within the PKR-binding region of NS5A, including those within the ISDR, can disrupt the NS5a-PKR interaction, possibly rendering HCV sensitive to the antiviral effects of interferon.
Arbidol: a broad-spectrum antiviral compound that blocks viral fusion.
TLDR
This review aims to compare various aspects of ARB anti-fusion mechanisms against influenza virus and HCV (with reference to different stringency of pH-dependence of these two viral fusogens) and to discuss further prospects for ARB and its improved derivatives of the parent compounds.
Hepatitis C virus NS5A colocalizes with the core protein on lipid droplets and interacts with apolipoproteins.
TLDR
An association of NS5A with lipid droplets and apoA1 is established, suggesting thatNS5A, together with the core protein, may play a role in the pathogenesis of the derangement of lipid metabolism, contributing to liver steatosis commonly observed in hepatitis C.
Hepatitis C Virus Nonstructural 5A Protein Induces Interleukin-8, Leading to Partial Inhibition of the Interferon-Induced Antiviral Response
TLDR
It is suggested that NS5A inhibits the antiviral actions of IFN by at least two mechanisms and the first evidence for a biological effect of the transcriptional activity of the NS5a protein is provided.
Subversion of Cell Signaling Pathways by Hepatitis C Virus Nonstructural 5A Protein via Interaction with Grb2 and P85 Phosphatidylinositol 3-Kinase
TLDR
A model in which NS5A interacts with Grb2 to inhibit mitogenic signaling while simultaneously promoting the PI3K-AKT cell survival pathway by interaction with p85PI3K is suggested, which may represent a crucial step in HCV persistence and pathogenesis.
Prospective Characterization of Full-Length Hepatitis C Virus NS5A Quasispecies during Induction and Combination Antiviral Therapy
TLDR
The relationship between NS5A mutations and selection pressures before and during antiviral therapy and virologic response to therapy were investigated and suggest that NS5a can perturb or evade the IFN-induced antiviral response using sequences outside of the putative ISDR.
Myeloid suppressor cells induced by hepatitis C virus suppress T‐cell responses through the production of reactive oxygen species
TLDR
It is suggested that HCV promotes the accumulation of CD33+ MDSC, resulting in ROS‐mediated suppression of T‐cell responsiveness, which may facilitate and maintain HCV persistent infection.
A Crucial Role for Kupffer Cell-Derived Galectin-9 in Regulation of T Cell Immunity in Hepatitis C Infection
TLDR
It is demonstrated that galectin-9 production by Kupffer cells links the innate and adaptive immune response, providing a potential novel immunotherapeutic target in this common viral infection.
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