导读：特鲁多研究所的一项新研究揭示了人体如何调控γ-疱疹病毒，该病毒被认为是多种癌症的诱因。一种白细胞（被称为CD8 T细胞）能调控γ-疱疹病毒在感染初始的活跃阶段和长期潜伏阶段之间的改变，这一机制成为该研究的关键点。
电子显微镜下的单个疱疹病毒
特鲁多Trudeau研究所的一项新研究揭示了人体如何调控γ-疱疹病毒，该病毒被认为是多种癌症的诱因。这项研究在玛西娅克曼博士的实验室中展开，将刊登在《免疫学》（Immunology）期刊上。研究人员发现，白细胞在调控γ-疱疹病毒感染中发挥作用，并用于某些癌症的预防和治疗。
在布莱克曼的研究中，一种白细胞（被称为CD8 T细胞）能调控γ-疱疹病毒在感染初始的活跃阶段和长期潜伏阶段之间的改变，这一机制成为该研究的关键点，并将有助于开发疗法以控制γ-疱疹病毒的感染以及防止病毒相关癌症的发生。
感染致癌病毒是癌症的一种诱发因素，如EB病毒和卡波济氏肉瘤相关的疱疹病毒等γ-疱疹病毒。超过95％的人群感染这类病毒中的1种或2种，对它们研究的重点是了解其感染周期以及大多数人的免疫系统对之如何调控。
γ-疱疹病毒的感染特点包括2个阶段。前期属于活跃阶段，免疫系统通过攻击病毒进行排异反应，然而，病毒在体内形成一种“逃避”免疫反应的生存机制，研究人员把这个过程称为隐性感染。在躲避期间，病毒以静止、不活跃的形式存在，有时候，它能重新活化和再次增殖，从而增加癌症发生的风险。
如果免疫系统在一些情况下受到抑制，如器官移植或艾滋病等疾病，癌症的发生机会大大增加。
全球的研究人员对这类病毒的本质提出一些重要问题，并在实验室内从事解答性研究，问题包括：病毒如何逃脱免疫反应从而延长潜伏期？人体中病毒的激活源是什么？我们能否开发出新疗法以调控病毒活化以及预防癌症的发生？
γ-Herpesvirus Reactivation Differentially Stimulates Epitope-Specific CD8 T Cell Responses
Michael L. Freeman, Claire E. Burkum, Meghan K. Jensen, David L. Woodlandand Marcia A. Blackman
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.
文献链接：https://www.jimmunol.org/content/early/2012/03/09/jimmunol.1102787.abstract
