Department of Molecular Microbiology and Immunology, University of Southern California, Keck School of Medicine, 2011 Zonal Avenue, HMR-401, Los Angeles, CA 90033, USA.
Department of Molecular Microbiology and Immunology, University of Southern California, Keck School of Medicine, 2011 Zonal Avenue, HMR-401, Los Angeles, CA 90033, USA.
Curr Opin Virol. 2022 Feb;52:244-249. doi: 10.1016/j.coviro.2021.12.010. Epub 2021 Dec 29.
To establish successful infection in cells, it is essential for hepatitis C virus (HCV) to overcome intracellular antiviral responses. The host cell mechanism that fights against the virus culminates in the production of interferons (IFNs), IFN-stimulated genes (ISGs) and pro-inflammatory cytokines as well as the induction of autophagy and apoptosis. HCV has developed multiple means to disrupt the host signaling pathways that lead to these antiviral responses. HCV impedes signaling pathways initiated by pattern-recognition receptors (PRRs), usurps and uses the antiviral autophagic response to enhance its replication, alters mitochondrial dynamics and metabolism to prevent cell death and attenuate IFN response, and dysregulates inflammasomal response to cause IFN resistance and immune tolerance. These effects of HCV allow HCV to successful replicate and persist in its host cells.
为了在细胞中建立成功的感染，丙型肝炎病毒 (HCV) 必须克服细胞内抗病毒反应。宿主细胞对抗病毒的机制最终导致干扰素 (IFN)、IFN 刺激基因 (ISG) 和促炎细胞因子的产生，以及自噬和细胞凋亡的诱导。HCV 已经开发出多种方法来破坏导致这些抗病毒反应的宿主信号通路。HCV 阻碍了模式识别受体 (PRR) 启动的信号通路，篡夺并利用抗病毒自噬反应来增强其复制，改变线粒体动力学和代谢以防止细胞死亡和减弱 IFN 反应，并使炎症小体反应失调以导致 IFN 抵抗和免疫耐受。这些 HCV 的作用使 HCV 能够在其宿主细胞中成功复制和持续存在。
