Planelles V, Bachelerie F, Jowett J B, Haislip A, Xie Y, Banooni P, Masuda T, Chen I S
Department of Microbiology and Immunology, UCLA School of Medicine 90094-1678, USA.
J Virol. 1995 Sep;69(9):5883-9. doi: 10.1128/JVI.69.9.5883-5889.1995.
We investigated the fate of human immunodeficiency virus type 1 (HIV-1) viral DNA in infected peripheral blood lymphocytes and immortalized T-cell lines by using a replication-defective HIV-1. We observed that integrated HIV-1 DNA and viral gene expression decrease over time. A frameshift mutation in vpr resulted in maintenance of the HIV-1 provirus and stable persistence of viral expression. Transfection of vpr together with the neomycin resistance gene in the absence of other viral genes decreased the formation of geneticin-resistant colonies, indicating either a cytotoxic or a cytostatic effect upon cells. Therefore, maintenance of HIV-1 infection within an infected proliferating population is due to two competing processes, the rate of viral spread and the degree of cell growth inhibition and/or death induced by Vpr.
我们使用复制缺陷型人类免疫缺陷病毒1型（HIV-1），研究了感染外周血淋巴细胞和永生化T细胞系中HIV-1病毒DNA的命运。我们观察到整合的HIV-1 DNA和病毒基因表达随时间下降。vpr中的移码突变导致HIV-1前病毒的维持和病毒表达的稳定持续。在没有其他病毒基因的情况下，将vpr与新霉素抗性基因一起转染可减少对遗传霉素抗性菌落的形成，表明对细胞有细胞毒性或细胞抑制作用。因此，HIV-1在感染的增殖群体中的维持是由于两个相互竞争的过程，即病毒传播速率以及Vpr诱导的细胞生长抑制和/或死亡程度。
