Shibata R, Maldarelli F, Siemon C, Matano T, Parta M, Miller G, Fredrickson T, Martin M A
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.
J Infect Dis. 1997 Aug;176(2):362-73. doi: 10.1086/514053.
Chimeric simian-human immunodeficiency viruses (SHIVs) carrying envelope glycoproteins derived from a T cell-macrophage dual-tropic primary isolate (human immunodeficiency virus type 1 [HIV-1] strain DH12) were constructed. When inoculated into macaque monkeys, SHIV(MD14) carrying simian immunodeficiency virus-derived nef established significantly higher virus loads than did SHIV(MD1), which contains the HIV-1 nef gene. Three patterns of CD4 cell depletion were observed in infected monkeys: exponential and irreversible loss to undetectable levels within 10 weeks of infection; marked reduction during acute infection followed by partial recovery and stabilization (lasting from 10 weeks to > 1 year), with a later decline to undetectable levels in some animals; and a transient loss during acute infection. The induced immunodeficiency was accompanied by CD4 cell counts of < 50 cells/microL and was associated with Pneumocystis carinii pneumonia, cytomegalovirus meningoencephalitis, lymphoid depletion, and thymic atrophy.
构建了嵌合型猿猴-人类免疫缺陷病毒（SHIV），其携带源自T细胞-巨噬细胞双嗜性原始分离株（1型人类免疫缺陷病毒[HIV-1]毒株DH12）的包膜糖蛋白。当接种到猕猴体内时，携带猿猴免疫缺陷病毒衍生nef基因的SHIV(MD14)所产生的病毒载量显著高于含有HIV-1 nef基因的SHIV(MD1)。在受感染的猴子中观察到三种CD4细胞耗竭模式：感染后10周内呈指数级且不可逆转地降至检测不到的水平；急性感染期间显著减少，随后部分恢复并稳定（持续10周以上至1年以上），部分动物后期又降至检测不到的水平；以及急性感染期间短暂减少。诱导的免疫缺陷伴随着CD4细胞计数低于50个细胞/微升，并与卡氏肺孢子虫肺炎、巨细胞病毒性脑膜脑炎、淋巴细胞耗竭和胸腺萎缩有关。
