DIVERSITY AND PATHOGENESIS OF SIVAGM

在它们的栖息地，30%-50%的非洲绿猴 对猴免疫缺陷病毒(SIV)有反应的抗体。 然而，加勒比海绿猴的SIV呈阴性。尽管有些人 圈养的猕猴被发现携带SIV和艾滋病，猕猴在 到目前为止，它们的亚洲原生栖息地也是SIV 不是。人类和非人灵长类慢病毒都是已知的 在个体HIV-2和SIVmac之间存在遗传差异 分离株，我们的分析表明， SIVagm的覆盖面之广令人惊讶。因此，拟议的研究具有 两个主要目标。一是继续寻找SIVagm分离株 与HIV-1、HIV-2或SIVmac密切相关的疾病。另一个是 要确定病毒和/或宿主因素是否在 这些病毒的致病机理和物种特异性。 将从非洲绿中获得更多的SIVagm分离株 来自非洲地理分散地区的猴子。病毒式传播 分离株将通过Gag-Poll基因特异性探针进行筛选。这个 与HIV-1、HIV-2或SIVagm分离株密切相关的病毒可能会导致 美国将确定导致艾滋病的慢病毒的来源 人类。 SIVagm和SIVagm的致病潜力和物种特异性 SIVmac将在同源和异源猴子身上进行检测 物种。这些分析将指导我们搜索病毒和 /或宿主因素对发病起重要作用。如果病毒因素 事实证明，将进行重要的尝试来定位病原体 通过产生杂交病毒、替换基因或 非致病菌株与致病菌株的区域 一个。如果所有试图确定病毒因素对 致病机制失败了，那么我们可能不得不得出结论 因素很重要。然后将尝试确定 目标细胞的差异，定义宿主反应和其他 寄主中的遗传因素。

In their native habitat, 30-50% of African green monkeys have antibodies reactive to simian immunodeficiency virus (SIV). However, Caribbean green monkeys are SIV negative. Although some macaques in captivity are found with SIV and AIDS, macaques in their native habitat of asia examined to date have also been SIV negative. Both human and non-human primate lentiviruses are know to be genetically divergent among individual HIV-2, and SIVmac isolates, our analysis indicate that the genetic diversity of SIVagm is amazingly extensive. Therefore the proposed studies have two major goals. One is to continue search for SIVagm isolates that are closely related to HIV-1, HIV-2, or SIVmac. The other is to determine whether viral and /or host factors are important in pathogenesis and species specificity of these viruses. Additional SIVagm isolates will be obtained form African green monkeys from geographically dispersed regions of Africa. The viral isolates will be screened by gag-pol gene-specific probes. The ones closely related to HIV-1, HIV-2, or SIVagm isolates may lead us to identify the origin of lentiviruses that cause AIDS in humans. The pathogenic potential and species specificity of SIVagm and SIVmac will be examined in homologous and heterologous monkey species. These analyses will direct us to search for viral and /or host factors important for pathogenesis. If the viral factors prove to be important attempts will be made to locate pathogenic determinants by generating hybrid viruses; replacing genes or regions of the non-pathogenic strains with that of the pathogenic ones. If all attempts to establish viral factor being important to pathogenesis have failed then we may have to conclude that host factors are important. Attempts will then be made to identify differences in target cells, define host responses and other genetic factors in the hosts.