Shibata R, Sakai H, Kawamura M, Tokunaga K, Adachi A
Department of Viral Oncology, Kyoto University, Japan.
J Gen Virol. 1995 Nov;76 ( Pt 11):2723-30. doi: 10.1099/0022-1317-76-11-2723.
The genetic and functional basis of the replication-defective nature of human immunodeficiency virus type 1 (HIV-1) in monkey cells was studied. By the generation and characterization of chimeras between HIV-1 and simian immunodeficiency virus, the sequence encompassing the 3' half of the long terminal repeat, gag and pol genes of HIV-1 was found to be responsible for the growth restriction. Early and late phases of HIV-1 replication in monkey cells were analysed in detail using several assay systems: transfection/coculture, transcomplementation between various proviral clones carrying the CAT gene and effector clones and evaluation of transcription and reverse transcription. All the data were consistent with the notion that HIV-1 replication is blocked at a very early stage(s) such as uncoating and/or reverse transcription in monkey cells.
对1型人类免疫缺陷病毒（HIV-1）在猴细胞中复制缺陷性质的遗传和功能基础进行了研究。通过构建HIV-1与猿猴免疫缺陷病毒之间的嵌合体并对其进行表征，发现HIV-1长末端重复序列3' 端的后半部分、gag和pol基因所包含的序列导致了生长限制。使用多种检测系统详细分析了HIV-1在猴细胞中的早期和晚期复制阶段：转染/共培养、携带CAT基因的各种原病毒克隆与效应克隆之间的反式互补以及转录和逆转录的评估。所有数据均与以下观点一致，即HIV-1在猴细胞中的复制在非常早期的阶段（如脱壳和/或逆转录）就被阻断。
