The molecular basis of HCV-mediated immune dysregulation.
Chronic hepatitis C virus (HCV) infection, which occurs in over 85% of patients and causes mild to severe liver disease, is a growing burden to health systems worldwide. The propensity of HCV to establish persistent infection suggests that the virus, which is non-cytopathic, has evolved one or more mechanisms aimed at evading host immunity. In addition to the appearance of quasispecies, which may arise under selective pressure during B and T cell responses, HCV gene products interact with host proteins in order to subvert immune surveillance. Gaining insight into these interactions may provide the basis for novel therapies aimed at preventing chronic HCV infection.
Eisen-Vandervelde
Audrey L
AL
Department of Microbiology, Pathology, Beirne Carter Center for Immunology Research, University of Virginia, Charlottesville, VA 22908, USA.
Yao
Zhi Qiang
ZQ
Hahn
Young S
YS
D000818:Animals; D003713:Dendritic Cells / Q000276:immunology; D016174:Hepacivirus / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014758:Viral Core Proteins / Q000276:immunology
D014758:Viral Core Proteins