Skip to main content
. 2012 Jan;86(1):513–526. doi: 10.1128/JVI.05425-11

Fig 8.

Fig 8

Effect of RS-1 on HIV-1 replication and integration in PBMC. (A) Effect of RS-1 treatment on hRAD51 DNA repair endogenous activity. Cells were incubated for 24 h with increasing concentrations of RS-1. The effect of RS-1 on hRAD51 activity was then checked by quantifying its ability to promote cisplatin resistance in a standard survival analysis, as reported above, with some adjustment due to the property of the primary cells. (B) Effect of RS-1 treatment on HIV-1 replication in PBMC. PBMC were incubated for 24 h in media containing various concentrations of cisplatin in the presence of RS-1. Drugs were then removed, and cell survival was evaluated by an MTT assay as described in Materials and Methods. The effect on HIV-1 replication of a 24-hour treatment of the infected cells with RS-1 prior to infection (MOI = 0.1) was measured by quantifying the genomic RNA released in the medium 48 h postinfection by quantitative PCR. (C) Effect of RS-1 on the amount of two-LTR circles. Total DNA and two-LTR circles were quantified by quantitative PCR as described in Materials and Methods for two effective concentrations of RS-1. (D) Effect of RS-1 on integrated viral DNA amount. Integrated DNA was measured by quantitative PCR as reported in Materials and Methods. One hundred percent corresponds to the integrated DNA quantification obtained without RS-1 treatment. All results are the means from at least three representative independent experiments ± standard deviations (error bars). A Student test was performed on serial values. *, P < 0.05; **, P < 0.005.