一项新的研究报告说，猴子中的某些**和遗传学特征可增加某种猴类**缺陷病毒（或称SIV）疫苗的有效性。由于SIV与人类**缺陷性病毒（或称HIV）有着密切的关系，这些发现支持这样的观念，即某些人可能带有某些基因或**系统的特征，使得他们能够比其他人更好地抵御HIV。
在创制一种有效的HIV疫苗的道路上所遭遇的一个主要障碍是，人们对某个特别的疫苗所产生的有益的**反应缺乏了解。迄今为止， 在HIV疫苗的试验中**显示出具有保护性效应的是在2003年至2006年间在泰国开展的RV144试验。
这里，Norman Letvin及其同事立志搞清楚类似的SIV疫苗究竟是如何阻止感染的。研究人员给一大群的恒河猴接种了SIV疫苗，接着在一个为其2个星期的时间段中，研究人员反复地给这些猴子注射低剂量的SIV。有一半的猴子产生了对SIV的抵御力，而另外一半的猴子则受到病毒的感染。
接下来，该研究团队在受到保护的猴子中观察了3个层面的**反应：细胞**反应、先天**反应以及抗体反应。这些猴子的细胞**反应和先天**反应没有受到疫苗的足够刺激以提供机体保护，但研究人员却在它们的抗体反应有引人注目发现。低浓度的中和抗体与抵御SIV能力的增加之间具有关联性。在受到疫苗保护的猴子体内的中和抗体能够与病毒结合并阻断其感染细胞的能力。
研究人员还发现了一种保护性的遗传预测因子：一种叫做TRIM5的基因。那些机体表达某种形式的TRIM5的猴子能够比没有该基因的猴子更好地抵抗病毒感染。这两种特质本身都能提供机体保护效应，但兼具基因和**特质的猴子能够得到疫苗的*佳保护。
这些结果凸显了在将来参加HIV疫苗试验的志愿者中仔细察看这些**和基因特质类型的必要性。
Immune and Genetic Correlates of VaccineProtection Against Mucosal Infection by SIV inMonkeysSci Transl Med 4 May 2011: Vol. 3, Issue 81, p. 81ra36
The RV144vaccine trial in Thailand demonstrated that an HIV vaccine couldprevent infection in humans and highlights the importance ofunderstanding protective immunity against HIV. We used a nonhumanprimate model to define immune and genetic mechanisms of protectionagainst mucosal infection by the simian immunodeficiency virus(SIV). A plasmid DNA prime/recombinant adenovirus serotype 5 (rAd5)boost vaccine regimen was evaluated for its ability to protectmonkeys from infection by SIVmac251 or SIVsmE660 isolates afterrepeat intrarectal challenges. Although this prime-boost vaccineregimen failed to protect against SIVmac251 infection, 50% ofvaccinated monkeys were protected from infection with SIVsmE660.Among SIVsmE660-infected animals, there was about a one-logreduction in peak plasma virus RNA in monkeys expressing the majorhistocompatibility complex class I allele Mamu-A*01,implicating cytotoxic T lymphocytes in the control of SIVreplication once infection is established. AmongMamu-A*01–negative monkeys challenged with SIVsmE660, noCD8+ T cell response or innate immune response wasassociated with protection against virus acquisition. However, lowlevels of neutralizing antibodies and an envelope-specificCD4+ T cell response were associated with vaccineprotection in these monkeys. Moreover, monkeys that expressed twoTRIM5 alleles that restrict SIV replication were morelikely to be protected from infection than monkeys that expressedat least one permissive TRIM5 allele. This study begins toelucidate the mechanisms of vaccine protection againstimmunodeficiency viruses and highlights the need to analyze theseimmune and genetic correlates of protection in future trials of HIVvaccine strategies.