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David R. Gretch

Researcher at University of Washington

Publications -  106
Citations -  11996

David R. Gretch is an academic researcher from University of Washington. The author has contributed to research in topics: Hepatitis C virus & Hepatitis C. The author has an hindex of 49, co-authored 106 publications receiving 11682 citations. Previous affiliations of David R. Gretch include Hirosaki University & University of Washington Medical Center.

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Hepatitis C Viral Dynamics in Vivo and the Antiviral Efficacy of Interferon-α Therapy

TL;DR: Findings show that infection with hepatitis C virus is highly dynamic and that early monitoring of viral load can help guide therapy, with blocking efficacies of 81, 95, and 96% for daily doses of 5, 10, and 15 million international units, respectively.
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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

TL;DR: 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.
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Control of PKR Protein Kinase by Hepatitis C Virus Nonstructural 5A Protein: Molecular Mechanisms of Kinase Regulation

TL;DR: 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.
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Diagnosis and Monitoring of Hepatic Injury. I. Performance Characteristics of Laboratory Tests

TL;DR: The international normalized ratio should not be the sole method for reporting results of prothrombin time in liver disease; additional research is needed to determine the reporting mechanism that best correlates with functional impairment.
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Negative Immune Regulator Tim-3 Is Overexpressed on T Cells in Hepatitis C Virus Infection and Its Blockade Rescues Dysfunctional CD4+ and CD8+ T Cells

TL;DR: For the first time, it is found that Tim-3 expression is increased on CD4+ and CD8+ T cells in chronic hepatitis C virus (HCV) infection and the ability to enhance T-cell proliferation and gamma interferon production in response to HCV-specific antigens by blocking the Tim- 3-Tim-3 ligand interaction is demonstrated.