Classic AIDS in a sooty mangabley after an 18-year natural infection
Classic AIDS in a sooty mangabley after an 18-year natural infection
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DOI：
10.1128/jvi.78.16.8902-8908.2004
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发表时间：
2004-08-01
影响因子：
5.4
通讯作者：
Marx, PA
中科院分区：
文献类型：
--
作者：
Ling, BH;Apetrei, C;Marx, PA
流行的理论认为，猿猴免疫缺陷病毒（SIV）感染在其天然猿猴宿主中是非致病性的，并且终身感染持续无疾病。许多研究报告说，SIV感染的白眉猴（SM; Cercocebus atys）保持疾病免费长达24年，尽管相对较高的病毒复制水平。在这里，我们报告说，典型的艾滋病发展后，18年的潜伏期在SM（E041）与自然SIVsm感染。与先前SM中SIV相关疾病的报道不同，感染E041的SIVsm并非首次通过猕猴传代;此外，SM E041是猴T细胞白血病病毒抗体阴性的。SM E041在2002年被诊断出患有严重的播散性B细胞淋巴瘤后被安乐死。血浆病毒载量在16年内大致相同，而在第17年和第18年病毒载量增加了100倍。与AIDS相关的其他发现包括CD 4+细胞减少、p27核心抗体缺失和SIVsm复制失控伴播散性巨细胞病。这些研究结果表明，艾滋病的发展时间超过了野生SM的平均寿命，SIV对其天然非洲宿主的主要适应并不包括对疾病的完全抵抗。相反，艾滋病可能发展缓慢，即使在病毒载量很高的情况下。然而，长期相对高的病毒载量，如SM E041中的病毒载量，与人类和猕猴中不到18年的艾滋病发展一致。因此，研究结果也表明SM具有抵抗艾滋病发展的特殊机制。
Prevailing theory holds that simian immunodeficiency virus (SIV) infections are nonpathogenic in their natural simian hosts and that lifelong infections persist without disease. Numerous studies have reported that SIV-infected sooty mangabeys (SMs; Cercocebus atys) remain disease free for up to 24 years despite relatively high levels of viral replication. Here, we report that classic AIDS developed after an 18-year incubation in an SM (E041) with a natural SIVsm infection. Unlike that described in previous reports of SIV-related disease in SMs, the SIVsm infecting E041 was not first passaged through macaques; moreover, SM E041 was simian T-cell leukemia virus antibody negative. SM E041 was euthanized in 2002 after being diagnosed with severe disseminated B-cell lymphoma. The plasma virus load had been approximately the same for 16 years when a 100-fold increase in virus load occurred in years 17 and 18. Additional findings associated with AIDS were CD4(+)-cell decline, loss of p27 core antibody, and loss of control of SIVsm replication with disseminated giant cell disease. These findings suggest that the time to development of AIDS exceeds the average lifetime of SMs in the wild and that the principal adaptation of SIV to its natural African hosts does not include complete resistance to disease. Instead, AIDS may develop slowly, even in the presence of high virus loads. However, a long-term relatively high virus load, such as that in SM E041, is consistent with AIDS development in less than 18 years in humans and macaques. Therefore, the results also suggest that SMs have a special mechanism for resisting AIDS development.