Figure 3
Figure 3. Kinetics of HIV-1 fusion and replication in cocultured MoDCs and primary autologous PHA-activated CD4 T lymphocytes. We added 5 μg/mL T20 (HIV-1 fusion inhibitor; A) or 5μM AZT (reverse transcriptase inhibitor; B) to HIV-1–loaded MoDCs/CD4 T lymphocytes cocultures at various times. Infection was assessed 48 hours after infection with HIV-1BaL and the percentage of infection compared with control (without T20 or AZT) was calculated. Data are expressed as means ± SD for n = 6 (A) or n = 4 (B) independent experiments performed with cells from different healthy blood donors. (C) Percentages of infection in each cocultured cell population in the presence of the HIV-1 protease inhibitor IDV compared with control cells (in the absence of IDV). Data are expressed as the means ± SD for n = 14 independent experiments performed with cells from different healthy blood donors.

Kinetics of HIV-1 fusion and replication in cocultured MoDCs and primary autologous PHA-activated CD4 T lymphocytes. We added 5 μg/mL T20 (HIV-1 fusion inhibitor; A) or 5μM AZT (reverse transcriptase inhibitor; B) to HIV-1–loaded MoDCs/CD4 T lymphocytes cocultures at various times. Infection was assessed 48 hours after infection with HIV-1BaL and the percentage of infection compared with control (without T20 or AZT) was calculated. Data are expressed as means ± SD for n = 6 (A) or n = 4 (B) independent experiments performed with cells from different healthy blood donors. (C) Percentages of infection in each cocultured cell population in the presence of the HIV-1 protease inhibitor IDV compared with control cells (in the absence of IDV). Data are expressed as the means ± SD for n = 14 independent experiments performed with cells from different healthy blood donors.

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