Otsyula M G, Miller C J, Marthas M L, Van Rompay K K, Collins J R, Pedersen N C, McChesney M B
School of Veterinary Medicine, University of California-Davis 95616-8542, USA.
Pediatr Res. 1996 Apr;39(4 Pt 1):630-5. doi: 10.1203/00006450-199604000-00012.
Six newborn rhesus macaques were experimentally infected with pathogenic Simian immunodeficiency virus of macaques (SIVmac251), and three newborn macaques were infected with avirulent SIVmac1A11. The former developed rapidly fatal simian AIDS and died within 26 wk of age, whereas the latter remained clinically normal. Infant monkeys that developed rapidly progressive disease had rapid declines in CD4+ cells and were unable to mount IgG and IgA antibody responses to SIV or to an unrelated antigen, tetanus toxoid. IgM antibody responses were near normal to both SIV-specific and nonspecific antigens. Cytotoxic T lymphocyte (CTL) responses to SIV envelope were observed in animals infected with either virulent or avirulent SIV. These studies demonstrated that virulent SIVmac infection induced a rapid immunosuppression that was both SIV-specific and nonspecific in nature. The observation that virulent strains of SIV can rapidly induce a global immunosuppression provides one explanation for the rapid disease course in some HIV-infected children and supports the strategy of early and vigorous antiviral drug therapy to alter the disease course even if this does not prevent infection.
六只新生恒河猴被实验性感染致病性猕猴免疫缺陷病毒（SIVmac251），三只新生猕猴被感染无毒力的SIVmac1A11。前者迅速发展为致命的猴艾滋病并在26周龄内死亡，而后者临床上保持正常。发展为快速进展性疾病的幼猴CD4 +细胞迅速减少，并且无法对SIV或无关抗原破伤风类毒素产生IgG和IgA抗体反应。对SIV特异性和非特异性抗原的IgM抗体反应接近正常。在感染了有毒力或无毒力SIV的动物中均观察到对SIV包膜的细胞毒性T淋巴细胞（CTL）反应。这些研究表明，有毒力的SIVmac感染会诱导快速的免疫抑制，这种免疫抑制在本质上既是SIV特异性的也是非特异性的。SIV的有毒力菌株可迅速诱导全身性免疫抑制这一观察结果为某些感染HIV的儿童疾病进展迅速提供了一种解释，并支持早期积极进行抗病毒药物治疗以改变疾病进程的策略，即使这不能预防感染。
