Duan L, Oakes J W, Ferraro A, Bagasra O, Pomerantz R J
Dorrance H. Hamilton Laboratories, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Virology. 1994 Mar;199(2):474-8. doi: 10.1006/viro.1994.1148.
Human immunodeficiency virus type 1 (HIV-1) can infect various cell lines in culture and be maintained in a chronic state of restricted replication. These states of proviral latency are characterized by a predominance of spliced compared to unspliced viral RNA species. The proximate molecular mechanisms leading to restricted HIV-1 replication may differ in various cell lines. Importantly, recent studies have demonstrated that the site of integration is the critical parameter leading to proviral latency in ACH-2 cells. Utilizing murine retroviral shuttle vectors, the HIV-1 Tat protein was demonstrated to dramatically increase HIV-1 expression in the restrictively infected U1 monocytic cell line but not in the ACH-2 T-lymphocytic line. The HIV-1 Rev protein only modestly increased viral expression in both of these cell types. Thus, these data support the hypothesis that the mechanisms which initiate and/or maintain restricted HIV-1 expression may differ in various cell types in cell culture, and possibly in vivo.
1型人类免疫缺陷病毒(HIV-1)可感染培养中的多种细胞系,并维持在复制受限的慢性状态。这些原病毒潜伏状态的特征是,与未剪接的病毒RNA种类相比,剪接后的病毒RNA占优势。导致HIV-1复制受限的直接分子机制在不同细胞系中可能有所不同。重要的是,最近的研究表明,整合位点是导致ACH-2细胞中病毒潜伏的关键参数。利用鼠逆转录病毒穿梭载体,已证明HIV-1 Tat蛋白可显著增加在限制性感染的U1单核细胞系中的HIV-1表达,但在ACH-2 T淋巴细胞系中则不然。HIV-1 Rev蛋白仅适度增加这两种细胞类型中的病毒表达。因此,这些数据支持这样一种假说,即启动和/或维持HIV-1表达受限的机制在细胞培养的不同细胞类型中可能不同,在体内也可能如此。