Pathogenesis of acute infection in rhesus macaques with a lymphocyte-tropic strain of simian immunodeficiency virus.
Pathogenesis of acute infection in rhesus macaques with a lymphocyte-tropic strain of simian immunodeficiency virus.
复制标题
猿猴免疫缺陷病毒嗜淋巴细胞株急性感染恒河猴的发病机制。
DOI：
10.1093/infdis/166.4.738
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Narayan,O
中科院分区：
文献类型：
--
作者：
Sharma,DP;Anderson,M;Zink,MC;Adams,RJ;Donnenberg,AD;Clements,JE;Narayan,O
猿猴免疫缺陷病毒 (SIVmac) 会引起影响猕猴多个器官系统的疾病，与人类感染人类免疫缺陷病毒类似。具有强淋巴细胞趋向性的分子克隆 SIVmac 用于发病机制实验，以将病毒细胞趋向性与疾病联系起来。在 5 只动物中，在感染过程中多次对组织中的病毒进行了详尽的分析，并鉴定了受感染的前体细胞，以确保病毒没有突变成嗜巨噬细胞的变体。通过感染性、感染中心测定和原位杂交来测量病毒复制。淋巴细胞在组织中产生大部分病毒，表明病毒在体内保持其细胞向性。骨髓中的淋巴细胞被潜伏感染，脾脏和淋巴结中的淋巴细胞被高效感染。脑内接种后，病毒未能在大脑中复制。 SIVmac对淋巴细胞保持较强的亲和性，而对巨噬细胞的亲和性相应较差，可导致恒河猴持续感染和艾滋病，但不会引起其他疾病，如原发性肺炎和脑炎。
The simian immunodeficiency virus, SIVmac, causes disease affecting multiple organ systems in macaques similar to human immunodeficiency virus infection in humans. Molecularly cloned SIVmacwith a strong lymphocyte tropism was used in pathogenesis experiments to correlate viral cell tropism with disease. In 5 animals, exhaustive analyses on viruses from tissues and identification of infected precursor cells were done at multiple times during infection to ensure the virus had not mutated into a macrophage-tropic variant. Viral replication was measured by infectivity, infectious center assays, and in situ hybridization. Lymphocytes produced most virus in tissues, indicating the virus maintained its cell tropism in vivo. Lymphocytes in bone marrow were latently infected and those in the spleen and lymph nodes were productively infected. The virus failed to replicate in the brain after intracerebral inoculation. SIVmac that maintained a strong tropism for lymphocytes and a corresponding poor tropism for macrophages can cause persistent infection and AIDS but not other diseases such as primary pneumonia and encephalitis in rhesus macaques.