Müller J G, Czub S, Marx A, Brinkmann R, Plesker R, Müller-Hermelink H K
Institute of Pathology, University of Würzburg, Germany.
Res Virol. 1994 May-Aug;145(3-4):239-44. doi: 10.1016/s0923-2516(07)80028-8.
To clarify the pathogenesis of SIV-induced thymus atrophy, the presence of SIV within thymus stromal cell cultures (epithelial cells, IDC, macrophages or fibroblasts) was investigated. The material studied consisted of 15 thymus specimens of rhesus macaques infected with SIVmac251 (2-4 months postinoculation). No viral antigen was detected, either in the cultures, by immunohistochemistry, or in cell culture supernatants, by ELISA (p17 antigen), and no viral RNA was detected by in situ hybridization. Only after coculture with the C8166 cell line, was virus detected in 2 out of 15 stroma cultures. The fact that the virus could only be detected after several passages of coculture with the C8166 cell line indicates that the virus exists in the thymus stroma cells in the form of proviral DNA. The infection of thymus stromal cells may contribute to the destruction of the thymus microenvironment and to the SIV-induced thymus atrophy.
为阐明SIV诱导胸腺萎缩的发病机制，研究了胸腺基质细胞培养物（上皮细胞、IDC、巨噬细胞或成纤维细胞）中SIV的存在情况。研究材料包括15份感染SIVmac251的恒河猴胸腺标本（接种后2 - 4个月）。通过免疫组织化学在培养物中未检测到病毒抗原，通过ELISA（p17抗原）在细胞培养上清液中也未检测到病毒抗原，且通过原位杂交未检测到病毒RNA。仅在与C8166细胞系共培养后，15份基质培养物中有2份检测到病毒。病毒仅在与C8166细胞系共培养数代后才能检测到这一事实表明，病毒以原病毒DNA的形式存在于胸腺基质细胞中。胸腺基质细胞的感染可能导致胸腺微环境的破坏以及SIV诱导的胸腺萎缩。
