IMMUNE MECHANISMS CONTROLLING SIV INFECTION

临床证据表明，细胞免疫在 用猴免疫缺陷病毒控制HIV-1复制 对猕猴(SIVmac)艾滋病动物模型的研究表明，病毒 CD8+淋巴细胞耗尽的猴子的复制没有得到控制 在原发SIVmac感染过程中清除CD8+淋巴细胞 猴子在慢性SIVmac感染期间导致一种戏剧性的 再次被抑制的病毒血症的增加与 SIVmac特异性CD8+T细胞的再生这些结果证实了 细胞免疫在控制HIV-1感染中的重要性 并支持疫苗接种方法，这些方法将引发这些免疫 预防感染的应对措施

Clinical evidence suggests that cellular immunity plays a role in controlling HIV-1 replication Using the simian immunodeficiency virus of macaques (SIVmac) animal model of AIDS, we show that virus replication was not controlled in monkeys depleted of CD8+ lymphocytes during primary SIVmac infection Eliminating CD8+ lymphocytes form monkeys during chronic SIVmac infection resulted in a and dramatic increase in viremia that was again suppressed coincident with the reappearance of SIVmac-specific CD8+ T cells These results confirm the importance of cell-mediated immunity in controlling HIV-1 infection and support vaccination approaches that will elicit these immune responses for preventing infection