Lerche N W, Marx P A, Osborn K G, Maul D H, Lowenstine L J, Bleviss M L, Moody P, Henrickson R V, Gardner M B
California Primate Research Center, University of California, Davis 95616.
J Natl Cancer Inst. 1987 Oct;79(4):847-54.
A 2.5-year epidemiologic study of a breeding group of rhesus monkeys (Macaca mulatta), which is a focus of endemic simian acquired immunodeficiency syndrome (SAIDS), demonstrated a strong association between the occurrence of SAIDS and infection with a type D retrovirus, SAIDS retrovirus serotype 1 (SRV-1). Of 23 healthy "tracer" juvenile rhesus monkeys, 19 (83%) died with SAIDS within 9 months of introduction into the resident SAIDS-endemic population. In contrast, 21 healthy "sentinel" juvenile rhesus monkeys placed in the same outdoor enclosure but denied physical contact with the SAIDS-affected group by a 10-foot-wide "buffer zone" remained free of SRV-1, SRV-1 antibody, and disease for 2.5 years. The SAIDS-specific mortality rate was significantly higher in juveniles than in adults. In repeated serologic testing, the overall prevalence of SRV-1 antibody ranged from 68 to 85%. Antibody prevalence increased with age. Seroconversion was found to be a poor indicator of infection rate, as approximately 50% of virus-positive juvenile monkeys had no antibody detectable by enzyme-linked immunosorbent assay. Repeated viral isolations from all animals revealed 1) SRV-1 viremia with clinical SAIDS; 2) persistent viremia and viral shedding in apparently healthy animals; 3) transient viremia and clinical recovery; 4) intermittent viremia, suggesting activation of latent infections; and 5) viremia in a 1-day-old infant, suggesting transplacental transmission. The prevalence of SRV-1 antibody in SAIDS-free breeding groups of rhesus monkeys was 4%. The seroprevalence of antibodies against human T-cell leukemia virus type 1 (HTLV-1), human immunodeficiency virus (HIV), and simian immunodeficiency virus (SIV; formerly STLV-III) was uniformly low or absent in both SAIDS-free and SAIDS-affected groups of rhesus monkeys, demonstrating that these retroviruses are not etiologically linked to SAIDS at the California Primate Research Center.
对一群恒河猴(猕猴)进行的为期2.5年的流行病学研究表明,猴获得性免疫缺陷综合征(SAIDS)的发生与感染D型逆转录病毒——SAIDS逆转录病毒1型(SRV-1)之间存在密切关联。该猴群是地方性SAIDS的研究重点。在23只健康的“追踪”幼年恒河猴中,19只(83%)在引入SAIDS地方性流行猴群后的9个月内死于SAIDS。相比之下,21只健康的“哨兵”幼年恒河猴被安置在同一个户外围栏中,但通过一个10英尺宽的“缓冲区”与受SAIDS影响的猴群隔离,在2.5年的时间里未感染SRV-1、未产生SRV-1抗体且未患病。SAIDS特异性死亡率在幼年猴中显著高于成年猴。在反复的血清学检测中,SRV-1抗体的总体患病率在68%至85%之间。抗体患病率随年龄增长而增加。血清转化被发现是感染率的一个不良指标,因为大约50%的病毒阳性幼年猴通过酶联免疫吸附测定法检测不到抗体。对所有动物反复进行病毒分离显示:1)患有临床SAIDS的SRV-1病毒血症;2)明显健康的动物中存在持续性病毒血症和病毒脱落;3)短暂性病毒血症和临床康复;4)间歇性病毒血症,提示潜伏感染激活;5)一只1日龄婴儿出现病毒血症,提示经胎盘传播。在无SAIDS的恒河猴繁殖群体中,SRV-1抗体的患病率为4%。在无SAIDS和受SAIDS影响的恒河猴群体中,针对人类T细胞白血病病毒1型(HTLV-1)、人类免疫缺陷病毒(HIV)和猴免疫缺陷病毒(SIV;原STLV-III)的抗体血清阳性率均一直很低或不存在,这表明在加利福尼亚灵长类动物研究中心,这些逆转录病毒与SAIDS在病因学上没有关联。