Guidotti L G, Chisari F V
Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California92037, USA.
Curr Opin Immunol. 1996 Aug;8(4):478-83. doi: 10.1016/s0952-7915(96)80034-3.
It is generally thought that viral clearance is mediated primarily by antigen-specific T cell responses that destroy infected cells. This assumption may not be true for all viruses. Recent studies using a transgenic mouse model of hepatitis B virus infection have shown that adoptively transferred, virus-specific cytotoxic T cells can abolish hepatitis B virus gene expression and replication in the liver without killing the hepatocytes. This effect is mediated by interferon-gamma and tumor necrosis factor-alpha, which are secreted by the cytotoxic T lymphocytes following antigen recognition. Similar noncytopathic cytokine-dependent 'curative' processes also occur in this model during an unrelated infection of the liver. Intracellular viral inactivation mechanisms such as these could greatly amplify the protective effects of the immune response. Research has also been carried out to clarify the relevance of curative versus destructive mechanisms of viral clearance in other models of viral infection.
一般认为，病毒清除主要由破坏受感染细胞的抗原特异性T细胞反应介导。这一假设可能并非对所有病毒都成立。最近利用乙型肝炎病毒感染的转基因小鼠模型进行的研究表明，过继转移的病毒特异性细胞毒性T细胞可在不杀死肝细胞的情况下消除肝脏中的乙型肝炎病毒基因表达和复制。这种效应由细胞毒性T淋巴细胞在识别抗原后分泌的干扰素-γ和肿瘤坏死因子-α介导。在肝脏的无关感染期间，该模型中也会发生类似的非细胞病变性细胞因子依赖性“治愈”过程。诸如此类的细胞内病毒灭活机制可极大地增强免疫反应的保护作用。人们还开展了研究，以阐明病毒清除的治愈机制与破坏机制在其他病毒感染模型中的相关性。
