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首页> 外文期刊>AIDS >Broadening of CD8+ cell responses in vaccine-based simian immunodeficiency virus controllers.
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Broadening of CD8+ cell responses in vaccine-based simian immunodeficiency virus controllers.

机译：在基于疫苗的猿猴免疫缺陷病毒控制者中扩大CD8 +细胞反应。

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OBJECTIVE: In our prior study on a prophylactic T-cell-based vaccine, some vaccinated macaques controlled a simian immunodeficiency virus (SIV) challenge. These animals allowed viremia in the acute phase but showed persistent viral control after the setpoint. Here, we examined the breadth of postchallenge virus-specific cellular immune responses in these SIV controllers. DESIGN: We previously reported that in a group of Burmese rhesus macaques possessing the MHC haplotype 90-120-Ia, immunization with a Gag-expressing vaccine results in nonsterile control of a challenge with SIVmac239 but not a mutant SIV carrying multiple cytotoxic T lymphocyte (CTL) escape gag mutations. In the present study, we investigated whether broader cellular immune responses effective against the mutant SIV replication are induced after challenge in those vaccinees that maintained wild-type SIVmac239 control. METHODS: We analyzed cellular immune responses in these SIV controllers (n = 8). RESULTS: These controllers elicited CTL responses directed against SIV non-Gag antigens as well as Gag in the chronic phase. Postvaccinated, prechallenge CD8(+) cells obtained from these animals suppressed wild-type SIV replication in vitro, but mostly had no suppressive effect on the mutant SIV replication, whereas CD8(+) cells in the chronic phase after challenge showed efficient antimutant SIV efficacy. The levels of in-vitro antimutant SIV efficacy of CD8(+) cells correlated with Vif-specific CD8(+) T-cell frequencies. Plasma viremia was kept undetectable even after the mutant SIV superchallenge in the chronic phase. CONCLUSION: These results suggest that vaccine-based wild-type SIV controllers can acquire CD8(+) cells with the potential to suppress replication of SIV variants carrying CTL escape mutations.
机译：目的：在我们先前对预防性T细胞疫苗的研究中，一些接种过猕猴控制了猿猴免疫缺陷病毒（SIV）攻击。这些动物在急性期允许病毒血症，但在设定值后表现出持续的病毒控制。在这里，我们检查了这些SIV控制器中攻击后病毒特异性细胞免疫应答的广度。设计：我们先前曾报道过，在一群拥有MHC单倍型90-120-Ia的缅甸恒河猴中，用表达Gag的疫苗免疫可对SIVmac239进行挑战的无菌控制，但不能对携带多细胞毒性T淋巴细胞的突变SIV进行控制（ CTL）逃避堵嘴突变。在本研究中，我们调查了在维持野生型SIVmac239对照的那些疫苗中，攻击后是否诱导了更有效的针对突变SIV复制的更广泛的细胞免疫应答。方法：我们分析了这些SIV控制器中的细胞免疫应答（n = 8）。结果：这些控制器引发针对SIV非Gag抗原以及慢性期的Gag的CTL反应。从这些动物获得的疫苗接种后的攻击前CD8（+）细胞在体外抑制了野生型SIV复制，但对突变SIV复制几乎没有抑制作用，而攻击后处于慢性期的CD8（+）细胞显示出有效的抗突变SIV功效。 CD8（+）细胞的体外抗突变SIV功效水平与Vif特异的CD8（+）T细胞频率相关。即使在慢性期发生突变型SIV超级挑战后，血浆病毒血症仍无法检测到。结论：这些结果表明基于疫苗的野生型SIV控制器可以获取CD8（+）细胞，具有抑制带有CTL逃逸突变的SIV变体复制的潜力。

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