丙型肝炎病毒诱导和逃避先天抗病毒反应。
Induction and evasion of innate antiviral responses by hepatitis C virus.
机构信息
Division of Infectious Disease, Department of Medicine, Center for Translational Immunology, Inflammatory Diseases Institute, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7030, USA.
出版信息
J Biol Chem. 2010 Jul 23;285(30):22741-7. doi: 10.1074/jbc.R109.099556. Epub 2010 May 10.
Abstract
Persistent hepatitis C virus infection is associated with progressive hepatic fibrosis and liver cancer. Acute infection evokes several distinct innate immune responses, but these are partially or completely countered by the virus. Hepatitis C virus proteins serve dual functions in replication and immune evasion, acting to disrupt cellular signaling pathways leading to interferon synthesis, subvert Jak-STAT signaling to limit expression of interferon-stimulated genes, and block antiviral activities of interferon-stimulated genes. The net effect is a multilayered evasion of innate immunity, which negatively influences the subsequent development of antigen-specific adaptive immunity, thereby contributing to virus persistence and resistance to therapy.
摘要
持续性丙型肝炎病毒感染与进行性肝纤维化和肝癌有关。急性感染会引发几种不同的固有免疫反应，但这些反应会被病毒部分或完全抵消。丙型肝炎病毒蛋白在复制和免疫逃逸中具有双重功能，作用是破坏导致干扰素合成的细胞信号通路，颠覆 Jak-STAT 信号以限制干扰素刺激基因的表达，并阻断干扰素刺激基因的抗病毒活性。其净效应是固有免疫的多层逃避，这会对随后的抗原特异性适应性免疫的发展产生负面影响，从而导致病毒持续存在和对治疗的耐药性。
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