Immunological features of murine gammaherpesvirus infection

Anthony A. Nash, Edward J. Usherwood, James P. Stewart
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引用次数: 26

Abstract

Murine gammaherpesvirus (MHV-68) represents a unique opportunity to explore the detailed interaction of a gammaherpesvirus with its natural host. In particular the immunological events occurring in the primary infection and in the establishment of latency are poorly understood. The virus infects experimental mice, replicating in the lung. Spread then occurs to the B-cell compartment resulting in splenomegaly, a process reminiscent of infectious mononucleosis in humans. The virus then becomes latent in B cells and persists. In addition, long-term infection is associated with the development of lymphoproliferative disease. We show here that CD8 T cells are key cells in resolving the primary infection and in maintaining the numbers of latently-infected B cells. A critical interplay exists between B cells and CD4 T cells in the genesis of splenomegaly and in the numbers of latently infected B cells. Cytokines are probably involved here and serve to induce cell expansion in the spleen. A number of genes have been identified and probes for the lytic and latent cycle are being developed. The use of recombinant proteins, recombinant viruses and knockout mice will facilitate the use of this model in the exploration of immunotherapeutic strategies to target lytic and latent infections by gammaherpesvirus.

小鼠γ疱疹病毒感染的免疫学特征
小鼠γ疱疹病毒(MHV-68)为探索γ疱疹病毒与其自然宿主的详细相互作用提供了独特的机会。特别是发生在原发感染和建立潜伏期的免疫事件了解甚少。这种病毒感染实验小鼠,在肺部复制。然后扩散到b细胞室,导致脾肿大,这一过程使人想起人类传染性单核细胞增多症。然后病毒潜伏在B细胞中并持续存在。此外,长期感染与淋巴细胞增生性疾病的发生有关。我们在这里表明CD8 T细胞是解决原发性感染和维持潜伏感染B细胞数量的关键细胞。在脾肿大的发生和潜伏感染B细胞的数量中,B细胞和CD4 T细胞之间存在一个关键的相互作用。细胞因子可能与此有关,并可诱导脾脏细胞扩增。许多基因已被鉴定,并且正在开发用于裂解和潜伏循环的探针。利用重组蛋白、重组病毒和敲除小鼠,将有助于利用该模型探索针对γ疱疹病毒裂解性和潜伏性感染的免疫治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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