INTERACTIONS BETWEEN SIMIAN AIDS (SAIDS) & LEPROSY

此前，8只恒河猴(RM)在同一天接种 SIV+麻风杆菌(ML)组；另4个对照RM仅接受ML。AS 前面提到，这些研究的临床结果是一致的。 与我们之前的观察结果一致，即SIV合并感染使RM 麻风的易患麻风病的去年，我们继续在临床上和 在这项实验中，对幸存的动物进行免疫监测，并 收集了纵向获得的持续免疫学数据， 进行了计算和绘制。到目前为止，8人中有7人感染了 死于猿猴艾滋病(SAID)(有一个例外-- 因为一个无关的临床问题而被实施安乐死 SAID-阴性，但麻风在接种地点呈阳性)。其中六个 7例SAIDs阳性的RM在接种地点出现麻风，1例出现麻风 正向传播到遥远的地点。幸存的RM拥有 播散性麻风病，但没有SAIDs的临床症状。总而言之，2 在8名混合感染的RM中，有5人患上了播散性麻风 ML接种后9个月内皮肤部位的变化 毫升。1月龄和2月龄仔猪皮肤ML接种部位的活检 无法在4个控件RM中的3个中显示大量ML 只接种ML。纵向免疫学研究表明， 所有4个只接种ML的人和一个幸存的人 SAID阴性/麻风阳性RM产生针对ML特异性的抗体 酚醛糖脂-I(PGL-I)抗原，但其余7例合并感染 RM未能产生抗PGL-I反应。所有8个合并感染的RM都是 ML前后明显的抗GP 120抗体反应 接种直到死亡前，或者，在剩余的情况下 在ML共接种数月后存活下来的混合感染的RM。 类似的对刀豆蛋白A的原始细胞反应以前也是正常的 ML接种，并在混合感染的RM中逐渐减少 ML后接种。这一数字也呈递减趋势。 ML合并感染后对来普明的原始反应随时间延长，但 不在仅有ML感染的RM中。数据表明，SIV引起了 体液免疫和细胞免疫显著降低 针对ML的隔间，进一步支持我们的临床 观察表明，SIV和ML的混合感染会增强 对麻风病的易感性，即麻风病可能是一种机会主义 SIV阳性动物的感染。去年，这些研究是 通过开始一项研究而扩大，在该研究中，18个RM被分为3个 一组接种SIV，2周后， 和ML一起。另一组同时接种SIV+ML 第三组仅给予ML。这些动物仍在水下 研究并应提供有关可能影响的信息 两种感染的相对时间对临床结果的影响。

Previously, 8 rhesus monkeys (RM) were inoculated on the same day with SIV + M. leprae (ML); another 4 control RM received only ML. As previously noted, clinical results of these studies were consistent with our prior observations, i.e., SIV coinfection renders RM more susceptible to leprosy. Last year, we continued to clinically and immunologically monitor the surviving animals in this experiment, and longitudinally-acquired continuing immunologic data were collected, calculated and plotted. To date, 7 of 8 of the coinfected group have died as a result of simian AIDS (SAIDS) (with one exception--a RM that was euthanized for an unrelated clinical problem and was SAIDS-negative, but leprosy-positive at inoculation sites). Six of the 7 SAIDS-positive RM had leprosy at inoculation sites and 1 had positive dissemination to distant sites. The surviving RM has disseminated leprosy, but no clinical signs of SAIDS. In summary, 2 of 8 coinfected RM developed disseminated leprosy and 5 had leprosy at dermal sites of ML inoculation within 9 months postinoculation with ML. Biopsies of dermal ML inoculation sites at 1 and 2 months PI failed to show significant numbers of ML in 3 of the 4 control RM inoculated with ML only. Longitudinal immunologic studies showed that all 4 ML-only inoculated and the one surviving SAIDS-negative/leprosy-positive RM made antibodies to ML-specific phenolic glycolipid-I (PGL-I) antigen, but the remaining 7 coinfected RM failed to make anti-PGL-I responses. All 8 coinfected RM made significant anti-Gp 120 antibody responses prior to and after ML inoculation until just prior to death or, in the case of the remaining surviving coinfected RM, to date many months after ML coinoculation. Similarly blastogenic responses to Concanavalin A were normal before ML inoculation and progressively diminished in the coinfected RM post-ML inoculation. There was also a progressive decrease in blastogenic responses to lepromin with time after ML coinfection, but not in the ML-only infected RM. The data show that SIV causes a significant specific reduction in both the humoral and cellular immune compartments towards ML, adding further support to our clinical observations suggesting that coinfection with SIV and ML enhances the susceptibility towards leprosy, i.e., leprosy can be an opportunistic infection in SIV-positive animals. Last year, these studies were enlarged by beginning a study in which 18 RM were divided into 3 groups of 6. One group was inoculated with SIV and, after 2 weeks, with ML. Another group was inoculated with SIV + ML at the same time and the third group was given ML alone. These animals remain under study and should provide information regarding the possible influence of the relative timing of the two infections on clinical outcome.