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. 2010 Oct 11;285(50):39314–39328. doi: 10.1074/jbc.M110.155275

FIGURE 2.

FIGURE 2.

C-A1 blocks HIV-1 integration. A, C8166 cells incubated with C-A1 (2 μm) or AMD3100 (10 nm), added at the indicated time points, infected with HIV-1 NL4.3, and analyzed by FACS 48 h post-infection after intracellular p24 CA immunostaining. Mean values ± S.D. are shown, n = 3. B, SupT1 cells infected with a VSV-G pseudotyped HIV-1 vector in the presence of 8 μm azidothymidine, 100 nm Raltegravir, or 4 μm C-A1; drugs were added at the indicated time post-infection and cells analyzed by FACS 24 h later. Data are representative of two independent experiments. C, SupT1 cells infected with a VSV-G pseudotyped HIV-1 vector and analyzed 24 h post-infection by FACS (left panel) and TaqMan qPCR to detect total viral DNA (middle panel) or two LTR circular viral DNAs (right panel). Mean values ± S.D. are shown, n = 3. Heat-inactivated virus gave no detectable signal. D, same cells shown in C were re-analyzed 2 weeks later by FACS (left panel), TaqMan qPCR to measure total viral DNA (middle panel), and Alu-LTR qPCR (right panel) to measure integrated proviruses. Mean values ± S.D. are shown, n = 3. E and F, same experiments as in C and D, but cells were treated with the indicated doses of Raltegravir for 24 h. Mean values ± S.D. are shown, n = 3.