J Immunol：人体如何控制能致癌病毒

2012年3月12日，据《每日科学》，来自特鲁多研究所的一项新研究阐明了人体如何控制γ-疱疹病毒（一类能导致多种癌症的病毒）。这项研究由Mike Freeman博士领导，研究结果即将刊登于新一期的《免疫学杂志》（Journal of Immunology）上。该研究描述了白细胞在控制γ-疱疹病毒感染中的作用，对治疗及预防某些类型的癌症具有重要意义。

能促成癌症形成的因素有很多，其中之一便是致癌病毒的感染，如γ-疱疹病毒、EB病毒、卡波济氏肉瘤等。全世界有超过95%的个体都会感染一个或两个这类病毒，所以了解这些病毒的感染周期及大多数个体中免疫反应如何控制这些病毒是非常重要的。

γ-疱疹病毒的感染有2个截然不同的阶段。在感染初期，即活跃期，免疫系统对病毒积极攻击。随后，病毒开发出一种聪明的机制来隐藏自己以逃避免疫系统，研究人员称这个过程为隐性感染。在隐性感染期间，病毒依然存在，但处于一种安静的、休眠的状态。偶尔，它也会重新开始活动并再次增殖，从而增加癌症发生的风险。

如果免疫系统功能很弱，则癌症发生的机会将大大增加，比如骨髓移植后处于免疫抑制的患者，或患有其它疾病，如AIDS。

世界各地的研究人员对这些病毒的性质提出了很多重要问题，同时也在各自的实验室里致力于解答这些问题。包括：病毒如何逃脱机体的免疫反应，以建立终身的潜伏？是什么因素触发了病毒在某些人中的复发？我们能否开发出疗法开控制这些病毒的复发及预防癌症的发生？

Blackman研究的关键性发现是，一种被称为CD8 T的白细胞，在病毒起始活跃阶段及长期潜伏感染之间对病毒的控制机制不同。这些新发现将加速开发一些疗法，来控制γ-疱疹病毒的感染，并防止病毒相关癌症的发生。（生物谷bioon.com）

doi:10.4049/%u200Bjimmunol.1102787
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γ-Herpesvirus Reactivation Differentially Stimulates Epitope-Specific CD8 T Cell Responses

Michael L. Freeman, Claire E. Burkum, Meghan K. Jensen, et al

Abstract：The γ-herpesviruses are characterized by their ability to establish lifelong latency. Subsequent immune suppression leads to viral reactivation from latency and the onset of a variety of pathologies, including lymphoproliferative disease and cancers. CD8 T cells play a key role in preventing reactivation of latent virus. Therefore, to develop effective therapeutic immune strategies, it is essential to understand the maintenance of CD8 T cell responses during latency. Because the γ-herpesviruses are highly species-specific and mice cannot be infected with the human pathogens, EBV or Kaposi's sarcoma-associated herpesvirus, we have used a natural rodent γ-herpesvirus experimental infection model, γ-herpesvirus-68. In this report, we show that during long-term latent infection, naive CD8 T cells are recruited into the ongoing immune response in an epitope-specific manner. When virus reactivation is induced in vivo, the recruitment of CD8 T cells for some, but not all, epitopes is enhanced. The variation in recruitment is not due to differences in epitope presentation. We also show that CD8 T cells that are newly stimulated during reactivation are functionally impaired compared with acutely stimulated cells in terms of cytokine production. Thus, our results demonstrate unexpected complexity in the response of CD8 T cells specific for different viral epitopes that were stimulated during acute infection, quiescent latency, and reactivation.