Steger K K, Dykhuizen M, Mitchen J L, Hinds P W, Preuninger B L, Wallace M, Thomson J, Montefiori D C, Lu Y, Pauza C D
Department of Pathology and Laboratory Medicine, University of Wisconsin Medical School, Madison 53706, USA.
J Virol. 1998 Feb;72(2):1600-5. doi: 10.1128/JVI.72.2.1600-1605.1998.
Simian-human immunodeficiency virus 89.6PD (SHIV89.6PD) was pathogenic after intrarectal inoculation of rhesus macaques. Infection was achieved with a minimum of 2,500 tissue culture infectious doses of cell-free virus stock, and there was no evidence for transient viremia in animals receiving subinfectious doses by the intrarectal route. Some animals experienced rapid progression of disease characterized by loss of greater than 90% of circulating CD4+ T cells, sustained decreases in CD20+ B cells, failure to elicit virus-binding antibodies in plasma, and high levels of antigenemia. Slower-progressing animals had moderate but varying losses of CD4+ T cells; showed increases in circulating CD20+ B cells; mounted vigorous responses to antibodies in plasma, including neutralizing antibodies; and had low or undetectable levels of antigenemia. Rapid progression led to death within 30 weeks after intrarectal inoculation. Plasma antigenemia at 2 weeks after inoculation (P < or = 0.002), B- and T-cell losses (P < or = 0.013), and failure to seroconvert (P < or = 0.005) were correlated statistically with rapid progression. Correlations were evident by 2 to 4 weeks after intrarectal SHIV inoculation, indicating that early events in the host-pathogen interaction determined the clinical outcome.
猿猴-人类免疫缺陷病毒89.6PD（SHIV89.6PD）经直肠接种恒河猴后具有致病性。用至少2500个组织培养感染剂量的无细胞病毒原液可实现感染，且经直肠途径接受亚感染剂量的动物没有短暂病毒血症的证据。一些动物疾病进展迅速，其特征为循环CD4+T细胞损失超过90%、CD20+B细胞持续减少、血浆中未能产生病毒结合抗体以及高水平的抗原血症。疾病进展较慢的动物CD4+T细胞有中度但不同程度的损失；循环CD20+B细胞增加；对血浆中的抗体产生强烈反应，包括中和抗体；且抗原血症水平较低或检测不到。疾病快速进展导致经直肠接种后30周内死亡。接种后2周时的血浆抗原血症（P≤0.002）、B细胞和T细胞损失（P≤0.013）以及未能发生血清转化（P≤0.005）与疾病快速进展在统计学上相关。在经直肠接种SHIV后2至4周相关性明显，表明宿主-病原体相互作用中的早期事件决定了临床结果。
