Figure 6. HSV-2 infection enhances HIV-1 replication in a RA-dependent manner.

Mock-, UV-HSV-2-, or Live HSV-2-treated DCs were loaded with HIV-1 and co-cultured with autologous CD4⁺ T cells for 3 to 7 days (A) or 5 days (B–E). A) The kinetics of infection is shown for 1 of 3 similar experiments. B) The fold changes (mean ± SEM of 15 independent experiments) in HIV-1 DNA copies/cell for the 3 conditions after 5 days of co-culture are shown relative to the MOCK controls (set as 1). C) The percentage of p24⁺CD4⁺ T cells within each α₄β₇ subset was measured 5 days after co-culture with the differently treated DCs. 1 of 3 independent experiments is shown. D) The fold changes (mean ± SEM, 4 independent experiments) in the HIV-1 copies/cell in presence (+) or absence (−) of the RARα antagonist are shown relative to the mock-treated controls (set as 1). One experiment, in which the HIV-1 infection was about 100 fold higher in the live HSV-2 condition compared to the mock treated, was excluded. In the excluded experiment the RARα antagonist did not reverse the HSV-2-infected DC enhancement effect (reduced by 20%). (*p<0.05, **<0.01, ***p≤0.001).