Hepatitis: Oldach DW

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A digest of articles written 1999 and later, on the topic "Hepatitis," originating from Planet Earth —» Oldach DW.  Display:  All Citations ·  All Abstracts
1 Retraction SOCS1 and SOCS3 are targeted by hepatitis C virus core/gC1qR ligation to inhibit T-cell function. free! 2006

Yao ZQ, Waggoner SN, Cruise MW, Hall C, Xie X, Oldach DW, Hahn YS. · Beirne Carter Center for Immunology Research, Department of Microbiology and Pathology, University of Virginia, Charlottesville, Virginia 22908, USA. · J Virol. · Pubmed #16873288 links to  free full text

This publication has no abstract.

2 Retraction SOCS1 and SOCS3 are targeted by hepatitis C virus core/gC1qR ligation to inhibit T-cell function. free! 2005

Yao ZQ, Waggoner SN, Cruise MW, Hall C, Xie X, Oldach DW, Hahn YS. · Beirne Carter Center for Immunology Research, Department of Microbiology and Pathology, University of Virginia, Charlottesville, VA 22908, USA. · J Virol. · Pubmed #16306613 links to  free full text

Abstract: T cells play an important role in the control of hepatitis C virus (HCV) infection. We have previously demonstrated that the HCV core inhibits T-cell responses through interaction with gC1qR. We show here that core proteins from chronic and resolved HCV patients differ in sequence, gC1qR-binding ability, and T-cell inhibition. Specifically, chronic core isolates bind to gC1qR more efficiently and inhibit T-cell proliferation as well as gamma interferon (IFN-gamma) production more profoundly than resolved core isolates. This inhibition is mediated by the disruption of STAT phosphorylation through the induction of SOCS molecules. Silencing either SOCS1 or SOCS3 by small interfering RNA dramatically augments the production of IFN-gamma in T cells, thereby abrogating the inhibitory effect of core. Additionally, the ability of core proteins from patients with chronic infections to induce SOCS proteins and suppress STAT activation greatly exceeds that of core proteins from patients with resolved infections. These results suggest that the HCV core/gC1qR-induced T-cell dysfunction involves the induction of SOCS, a powerful inhibitor of cytokine signaling, which represents a novel mechanism by which a virus usurps the host machinery for persistence.