2012年3月12日,，據(jù)《每日科學(xué)》，來(lái)自特魯多研究所的一項(xiàng)新研究闡明了人體如何控制γ-皰疹病毒（一類能導(dǎo)致多種癌癥的病毒）,。這項(xiàng)研究由Mike Freeman博士領(lǐng)導(dǎo),，研究結(jié)果即將刊登于新一期的《免疫學(xué)雜志》（Journal of Immunology）上,。該研究描述了白細(xì)胞在控制γ-皰疹病毒感染中的作用,，對(duì)治療及預(yù)防某些類型的癌癥具有重要意義。
能促成癌癥形成的因素有很多,，其中之一便是致癌病毒的感染,，如γ-皰疹病毒、EB病毒,、卡波濟(jì)氏肉瘤等,。全世界有超過(guò)95%的個(gè)體都會(huì)感染一個(gè)或兩個(gè)這類病毒，所以了解這些病毒的感染周期及大多數(shù)個(gè)體中免疫反應(yīng)如何控制這些病毒是非常重要的,。
γ-皰疹病毒的感染有2個(gè)截然不同的階段,。在感染初期，即活躍期,，免疫系統(tǒng)對(duì)病毒積極攻擊,。隨后，病毒開(kāi)發(fā)出一種聰明的機(jī)制來(lái)隱藏自己以逃避免疫系統(tǒng),，研究人員稱這個(gè)過(guò)程為隱性感染,。在隱性感染期間，病毒依然存在,，但處于一種安靜的,、休眠的狀態(tài)。偶爾,，它也會(huì)重新開(kāi)始活動(dòng)并再次增殖,，從而增加癌癥發(fā)生的風(fēng)險(xiǎn),。
如果免疫系統(tǒng)功能很弱，則癌癥發(fā)生的機(jī)會(huì)將大大增加,，比如骨髓移植后處于免疫抑制的患者,，或患有其它疾病，如AIDS,。
世界各地的研究人員對(duì)這些病毒的性質(zhì)提出了很多重要問(wèn)題,，同時(shí)也在各自的實(shí)驗(yàn)室里致力于解答這些問(wèn)題。包括：病毒如何逃脫機(jī)體的免疫反應(yīng),，以建立終身的潛伏,？是什么因素觸發(fā)了病毒在某些人中的復(fù)發(fā)？我們能否開(kāi)發(fā)出療法開(kāi)控制這些病毒的復(fù)發(fā)及預(yù)防癌癥的發(fā)生,？
Blackman研究的關(guān)鍵性發(fā)現(xiàn)是,，一種被稱為CD8 T的白細(xì)胞，在病毒起始活躍階段及長(zhǎng)期潛伏感染之間對(duì)病毒的控制機(jī)制不同,。這些新發(fā)現(xiàn)將加速開(kāi)發(fā)一些療法,，來(lái)控制γ-皰疹病毒的感染，并防止病毒相關(guān)癌癥的發(fā)生,。（生物谷bioon.com）
doi:10.4049/%u200Bjimmunol.1102787
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PMID:
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.
