INTERACTIONS BETWEEN SIMIAN AIDS (SAIDS) & LEPROSY

此前，8只恒河猴（RM）在同一天接种 SIV + M。对照组4例，仅接受ML治疗。 作为 如前所述，这些研究的临床结果一致 与我们先前的观察结果相一致，即，SIV合并感染使RM更多 易患麻风病的 去年，我们继续在临床上， 免疫学监测本实验中存活的动物， 收集患者获得的持续免疫学数据， 计算和绘制。 到目前为止，8名合并感染者中有7名 死于猿类艾滋病（SAIDS）（只有一个例外-一个RM， 因为一个无关的临床问题而被安乐死， SAIDS阴性，但在接种部位麻风病阳性）。 六 7例SAIDS阳性RM在接种点有麻风病，1例在接种点有麻风病， 积极传播到遥远的地方。 幸存的RM 播散性麻风，但没有SAIDS的临床症状。 总之，2 8例RM合并感染者中有5例发生播散型麻风， 接种后9个月内ML接种的皮肤部位， ML. PI 1和2个月时皮肤ML接种部位的活检 在4个对照RM中的3个中未显示显著数量的ML 仅接种ML。 纵向免疫学研究表明， 所有4个仅接种的mL和1个存活的mL SAIDS阴性/麻风病阳性RM产生针对ML特异性 酚糖脂-I（PGL-I）抗原，但其余7个共感染 RM未能产生抗PGL-I应答。 所有8例合并感染的RM ML之前和之后出现显着的抗Gp 120抗体反应 在死亡之前接种，或者在剩余的情况下， 存活的共感染RM，到ML共接种后数月为止。 类似地，对伴刀豆球蛋白A的胚细胞生成反应在 ML接种和进行性减少，在共感染RM ML接种后。 此外， ML合并感染后，随着时间的推移，对麻风菌素的胚细胞生成反应，但 而不是在仅感染ML的RM中。 数据显示，SIV导致 体液免疫和细胞免疫的显著特异性降低 为我们的临床研究提供进一步的支持。 观察结果表明，SIV和ML的共同感染增强了 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 通过将18个RM分成3个 6组。 一组接种SIV，2周后， 关于ML 另一组同时接种SIV + ML 而第三组仅给予ML。 这些动物仍在 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.