Herpesvirus saimiri as a model for gammaherpesvirus oncogenesis
Herpesvirus saimiri as a model for gammaherpesvirus oncogenesis
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DOI：
10.1006/scbi.1998.0115
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发表时间：
1999-06-01
影响因子：
14.5
通讯作者：
Biesinger, B
中科院分区：
文献类型：
--
作者：
Jung, JU;Choi, JK;Biesinger, B
赛米尔疱疹病毒 (HVS) 会导致一些新世界和旧世界灵长类动物以及某些兔子出现 T 淋巴细胞增殖性疾病。体外感染导致灵长类和人类来源的原代 T 细胞永久生长。 HVS 的转化相关蛋白与细胞原癌蛋白相互作用，导致细胞生长转化。此外，病毒编码的细胞同源物可能通过改变细胞信号转导和解除细胞生长控制来促进 HVS 的转化或持续存在。由于存在允许的细胞培养系统以及体外和体内转化测定，HVS 提供了一个独特的机会来研究致癌疱疹病毒诱导癌症的机制。
Herpesvirus saimiri (HVS) causes T-lymphoproliferative disorders in several New World and Old World primate species and in certain rabbits. In vitro infection leads to permanent growth of primary T cells of primate and human origins. The transformation-relevant proteins of HVS interact with cellular proto-oncoproteins which results in cell growth transformation. In addition, virus-encoded cellular homologues may contribute to transformation or persistence of HVS by altering cellular signal transduction and deregulating cell growth control. Because of the presence of a permissive cell culture system and in vitro and in vivo transformation assays, HVS provides a unique opportunity to investigate the mechanisms of cancer induction by oncogenic herpesviruses.