據(jù)一項(xiàng)新的研究披露,，一種經(jīng)過(guò)設(shè)計(jì)的巨細(xì)胞病毒（CMV）根本性地改變了T細(xì)胞保護(hù)恒河猴免于SIV感染的活性,；猴子中的SIV相當(dāng)于人類的HIV。
Scott Hansen及其同事曾在近期報(bào)告了經(jīng)過(guò)設(shè)計(jì)可表達(dá)某些SIV蛋白的CMV株，從而讓得到疫苗接種的猴子能夠控制SIV感染,，現(xiàn)在他們又報(bào)告說(shuō)，這種特別的疫苗載體會(huì)驅(qū)使出一種來(lái)自CD8+ T細(xì)胞的非常獨(dú)特的免疫反應(yīng),。他們說(shuō),，當(dāng)與設(shè)計(jì)的被稱作68-1 RhCMV的CMV株相遇時(shí)，CD8+ T細(xì)胞會(huì)發(fā)動(dòng)一種比其通常的對(duì)SIV的免疫反應(yīng)強(qiáng)得多的反應(yīng),。在68-1 RhCMV存在的情況下,，CD8+ T細(xì)胞能夠?qū)IV的抗原表位——或者說(shuō)是抗原性蛋白的小片段——作為其標(biāo)靶，而這些抗原性表位通常會(huì)避開由其它經(jīng)過(guò)設(shè)計(jì)的病毒載體或僅由SIV感染所激發(fā)的免疫反應(yīng),。據(jù)研究人員披露,，CD8+ T細(xì)胞通常只對(duì)由屬于I類主要組織相容性復(fù)合物——或MHC-I——的細(xì)胞所呈現(xiàn)的抗原起反應(yīng)，但68-1 RhCMV產(chǎn)生了對(duì)MHC-I 和 MHC-II 分子都起反應(yīng)的CD8+ T細(xì)胞反應(yīng),。
他們的結(jié)果表明,，CMV載體可通過(guò)以遺傳編程從而讓它們能夠識(shí)別更廣泛的SIV抗原表位范圍這樣一種方法來(lái)影響CD8+ T細(xì)胞。這些發(fā)現(xiàn)可能最終會(huì)導(dǎo)致針對(duì)HIV治療的更為有效的手段,，而由Nilu Goonetilleke及Andrew McMichael撰寫的一篇《觀點(diǎn)欄目》文章更為詳細(xì)地解釋了這些結(jié)果,。(生物谷Bioon.com)
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Science DOI: 10.1126/science.123787
Cytomegalovirus Vectors Violate CD8+ T Cell Epitope Recognition Paradigms
CD8+ T cell responses focus on a small fraction of total pathogen-encoded peptides, which are similar among individuals with shared major histocompatibility complex (MHC) alleles. This focus can limit immune control of genetically flexible pathogens, such as HIV and SIV, because CD8+ T cells in most infected subjects do not target sequences required for pathogen fitness, resulting in viral escape. Although a vaccine capable of broadening or redirecting CD8+ T cell epitope targeting to prevent viral escape would be highly advantageous, it remains unclear whether this targeting can be diverted from its default pattern during priming.
