INDUCTION OF SUPEROVULATION & OOCYTE RECOVERY IN TWO SPECIES OF MACAQUES

这个试点项目的目标是确定源头 在SIV感染的猴子中感染禽分枝杆菌的特征 疾病的免疫相关性，并确定其可行性 预防SAID动物机会性感染的疫苗接种 阿维氏支原体。SAID人群中禽支原体感染(MAI)的发生率 菌落从1988年检测不到的水平增加到18%-25% 最近几年。这种机会性感染会导致腹泻， 恶病质，有时是肺炎，免疫功能严重受损 猴子在艾滋病儿童中与MAI有显著的相似性。我们 用培养和聚合酶链式反应检测禽类分枝杆菌 环境(土壤和水)和猴子的分子指纹图谱 分析。到目前为止，从环境中分离出来的菌株很少会深度感染 猴子的组织。猴巨噬细胞的体外检测 表明混合感染SIV和一种常见的SIV菌株的细胞 在我们的猴群中发现的致病性禽类分支杆菌产量高于 预期的病毒水平。我们致病病毒的蛋白质成分 正在对菌株进行表征。我们已经证明了动物 感染SIV和严重免疫缺陷的人可能会感染 我们的致病菌株(MavK128)在接种人类菌株时 禽型支原体(Serovar 4)不能感染免疫缺陷的猴子。在一个 四种动物接种超声灭活禽支原体的初步研究 SIV感染未能保护他们免受MavK128的挑战 但病变中含有比预期更多的淋巴细胞。未来研究 可以寻找有前景的禽类分支杆菌和佐剂的配方 可能对机会性感染提供保护。资金来源 风险研究出版物格林伯格SS，谢俊明，Kolls J，Mason C Didier P.大鼠一氧化氮合酶II基因的快速诱导 分枝杆菌气管内给药引起的肺泡巨噬细胞 结核病和禽类分枝杆菌。Proc Soc Exp Bio Med， 209：46-53,1995。首页--期刊主要分类--期刊细介绍--期刊题录与期刊详细文摘内容 用聚合酶链式反应检测恒河猴体内的禽类支原体。[摘要#2486]。FASE B J， 10(6)：A1431,1996。首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容 马斯洛JN.禽分枝杆菌复合体(MAC)感染的流行情况 在感染SIV的猴子身上。[摘要]。传染病学会 会议，1996年9月，洛杉矶新奥尔良。布拉尔一世，迪迪埃·P Murphey-Corb M，Maslow JN.禽分枝杆菌的流行病学研究 猴免疫缺陷病毒(SIV)复合(MAC)感染 被感染的恒河猴。[摘要#655]，p185，第4次会议 逆转录病毒和机会性感染，华盛顿特区，1月 22-26,1997年。

The objectives of this pilot project are to establish the source of Mycobacterium avium infection in SIV-infected monkeys, characterize immune correlates of disease, and determine the feasibility of vaccination to prevent opportunistic infection of SAIDS animals with M. avium. The incidence of M. avium infection (MAI) in the SAIDS colony has increased from undetectable levels in 1988 to 18-25% in recent years. This opportunistic infection produces diarrhea, cachexia, and sometimes pneumonia in severely immunocompromized monkeys with remarkable similarity to MAI in children with AIDS. We detect M. avium by culture and PCR and characterize isolates from the environment (soil and water) and monkeys by molecular fingerprint analysis. To date, isolates from the environment rarely infect deep tissues of monkeys. In vitro testing of monkey macrophages demonstrates that cells co-infected with SIV and a common strain of pathogenic M. avium found in our monkey colony produces higher than expecte d levels of virus. Protein components of our pathogenic strain are being characterized. We have demonstrated that animals infected with SIV and severely immunodeficient can be infected with our pathogenic strain (MavK128) while inoculation with a human strain of M. avium (Serovar 4) fails to infect immunodeficient monkeys. In a pilot study vaccination of four animals with sonicated M. avium prior to SIV-infection failed to protect them from challenge with MavK128 but lesions contained more lymphocytes than expected. Future studies could look for promising formulations of M. avium and adjuvant that might provide protection against opportunistic infection. FUNDING Venture Research PUBLICATIONS Greenberg SS, Xie JM, Kolls J, Mason C, Didier P. Rapid induction of mRNA for nitric oxide synthase II in rat alveolar macrophages by intratracheal administration of Mycobacterium tuberculosis and Mycobacterium avium. Proc Soc Exp Bio Med, 209:46-53, 1995. Didier P, Ramesh G, Newman G, Maslow J. Detection of M. avium by PCR in rhesus monkeys. [Abstract #2486]. FASEB J, 10(6):A1431, 1996. Brar I, Didier P, Murphey-Corb M, Newman GW, Maslow JN. Prevalence of Mycobacterium avium complex (MAC) infection in SIV infected monkeys. [Abstract]. Infectious Diseases Society Meeting, September 1996, New Orleans, LA. Brar I, Didier P, Murphey-Corb M, Maslow JN. Epidemiology of Mycobacterium avium complex (MAC) infection in simian immunodeficiency virus (SIV) infected rhesus monkeys. [Abstract #655], p185, 4th Conference on Retroviruses and Opportunistic Infections, Washington, DC, January 22-26, 1997.