Figure 2
Figure 2. Increased susceptibility of p PBMCs to R5 and X4 HIV-1 infection. PHA-activated PBMCs or PHA/IL-2–activated PBMCs were infected with R5 or X4 HIV-1 strains. HIV-1 propagation was monitored by p24gag antigen up to 25 days after infection, and plotted as a function of time. (A) R5 HIV-1Ba-L (0.5 ng HIV p24gag/5 × 105 cells). (B) X4 HIV-1IIIB (MOI, 0.3). (C) R5 HIV-1Ada-M (13.3ng of HIV p24gag/5 × 105 cells), R5 HIV-1JR-FL (3.25 ng HIV p24gag/ 5 × 105 cells). (D) X4 HIV-1NL4-3 gp41 36G (11.6 ng HIV p24gag/ 5 × 105 cells). (C,D) Fold change was calculated for each p donor (p1, p2, and p3) based on control infection levels of samples taken at the last time point. Data are representative of the mean ± SEM, where n = 4 infection data points, *P < .05, **P < .002. ◇ represents healthy PBMCs controls designated C-p1, C-p2, or C-p3 (Table 3); (■), p PBMCs designated p1, p2, or p3 (Table 2).

Increased susceptibility of p PBMCs to R5 and X4 HIV-1 infection. PHA-activated PBMCs or PHA/IL-2–activated PBMCs were infected with R5 or X4 HIV-1 strains. HIV-1 propagation was monitored by p24gag antigen up to 25 days after infection, and plotted as a function of time. (A) R5 HIV-1Ba-L (0.5 ng HIV p24gag/5 × 105 cells). (B) X4 HIV-1IIIB (MOI, 0.3). (C) R5 HIV-1Ada-M (13.3ng of HIV p24gag/5 × 105 cells), R5 HIV-1JR-FL (3.25 ng HIV p24gag/ 5 × 105 cells). (D) X4 HIV-1NL4-3 gp41 36G (11.6 ng HIV p24gag/ 5 × 105 cells). (C,D) Fold change was calculated for each p donor (p1, p2, and p3) based on control infection levels of samples taken at the last time point. Data are representative of the mean ± SEM, where n = 4 infection data points, *P < .05, **P < .002. ◇ represents healthy PBMCs controls designated C-p1, C-p2, or C-p3 (Table 3); (■), p PBMCs designated p1, p2, or p3 (Table 2).

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