Hein A, Martin J P, Dörries R
Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Mannheim, Ruprecht-Karls-Universität Heidelberg, Mannheim, Germany.
J Virol. 2001 Sep;75(17):8090-5. doi: 10.1128/jvi.75.17.8090-8095.2001.
Intravenous infection of cats with feline immunodeficiency virus was used as a model system to study activation of virus replication in brain-resident microglial cells in vitro. Virus release by ramified microglial cells isolated from subclinically infected animals was detectable in cell-free tissue culture supernatant only by reverse transcription and nested PCR of gag-specific RNA sequences and not by virion-associated reverse transcriptase activity. In contrast, cocultivation of in vivo-infected microglial cells with mitogen-activated peripheral blood mononuclear cells (PBMC) regularly allows detection of high virus yields in cell-free tissue culture fluid. Besides uptake and multiplication of microglia-derived virus in PBMC, release of virus from microglia is stimulated by cell contact with PBMC. The data suggest that T lymphocytes patrolling the central nervous system could reactivate the semilatent state of lentiviruses in microglial cells in the course of clinically silent central nervous system infection.
将猫免疫缺陷病毒静脉注射感染猫，以此作为模型系统，用于体外研究脑内常驻小胶质细胞中病毒复制的激活情况。从亚临床感染动物分离出的分支状小胶质细胞释放的病毒，仅通过对gag特异性RNA序列进行逆转录和巢式PCR才能在无细胞组织培养上清液中检测到，而通过病毒粒子相关的逆转录酶活性则无法检测到。相比之下，将体内感染的小胶质细胞与丝裂原激活的外周血单核细胞（PBMC）共培养，通常能在无细胞组织培养液中检测到高病毒产量。除了PBMC摄取和繁殖小胶质细胞衍生的病毒外，小胶质细胞与PBMC的细胞接触会刺激病毒从小胶质细胞中释放。数据表明，在临床无症状的中枢神经系统感染过程中，巡逻于中枢神经系统的T淋巴细胞可能会重新激活小胶质细胞中慢病毒的半潜伏状态。
