Unraveling immunity to gamma-herpesviruses: a new model for understanding the role of immunity in chronic virus infection.
Unraveling immunity to gamma-herpesviruses: a new model for understanding the role of immunity in chronic virus infection.
复制标题
揭示对γ-疱疹病毒的免疫力：了解免疫在慢性病毒感染中的作用的新模型。
DOI：
10.1016/s0952-7915(99)80063-6
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发表时间：
1999
影响因子：
7
通讯作者：
Speck,SH
中科院分区：
文献类型：
--
作者：
Virgin,HW;Speck,SH
小鼠γ-疱疹病毒68（γ HV68）感染是了解免疫与慢性γ-疱疹病毒感染相互关系的新模型。γ HV 68与人类EB病毒和卡波西肉瘤疱疹病毒密切相关，并与肿瘤、大弹性动脉血管炎和脾纤维化有关。过去一年的进展为相信γ HV 68感染正常和突变小鼠将成为了解γ-疱疹病毒发病机制和免疫的卓越动物模型提供了更有力的基础。采用新的测定方法对γ HV 68潜伏期进行了表征，这些方法用于定量携带γ HV 68基因组的细胞和重新激活γ HV 68的细胞，并用于检测组织中是否存在预先形成的感染性病毒。这些进展为γ HV 68潜伏期的分子定义迈出了第一步。γ HV 68似乎与人类γ疱疹病毒共享潜伏程序-包括基因73、v-bcl-2和G蛋白偶联受体的病毒同系物的位点。这为分析T和B细胞在调节潜伏期中的作用提供了候选抗原。发现了γ HV 68潜伏期的多个细胞储库，证明γ HV 68除了B细胞外还潜伏感染巨噬细胞。人们发现B细胞在调节γ HV 68潜伏期的性质方面发挥着关键作用，其机制被证明是通过改变再激活的效率。对急、慢性γ HV 68过程中CD4+、CD8+细胞的反应进行了研究。这些新的研究为进一步开发这种新颖有趣的模型系统提供了关键的构建模块。
Murine γ-herpesvirus 68 (γHV68) infection is a new model for understanding how immunity and chronic γ-herpesvirus infection inter-relate. γHV68 is closely related to the human Epstein-Barr virus and Kaposi's sarcoma herpesvirus and is associated with tumors, vasculitis of the great elastic arteries and splenic fibrosis. Advances in the past year have provided an even stronger foundation for believing that γHV68 infection of normal and mutant mice will become the pre-eminent animal model for understanding γ-herpesvirus pathogenesis and immunity. γHV68 latency has been characterized employing new assays for quantitating cells carrying the γHV68 genome and cells that reactivate γHV68 and for detecting the presence of preformed infectious virus in tissues. These advances have fostered the first steps towards a molecular definition of γHV68 latency. It appears that γHV68 shares latency programs with human γ-herpesviruses — including the loci for gene 73, v-bcl-2 and the viral homolog of the G-protein coupled receptor. This provides candidate antigens for analysis of the role of T and B cells in regulating latency. Multiple cellular reservoirs for γHV68 latency were uncovered with the demonstration that γHV68 latently infects macrophages in addition to B cells. A critical role for B cells in regulating the nature of γHV68 latency was discovered and the mechanism was shown to be via alteration of the efficiency of reactivation. Studies of the response of CD4+and CD8+cells during acute and chronic γHV68 were performed. These new studies provide key building blocks for further development of this novel and interesting model system.