Figure 7.
Figure 7. DCs promote infection of HS CD4+ cells. (A) Susceptibility of HS and control CD4+ clones to HIV replication. As a positive control for viral replication, 2 HS clones (L11 and N2) and 2 control clones with other antigenic specificities (3.8, 2.2) were activated with PHA and grown with IL-2. Cells were infected at a high moi (2 nM p24 for 3 × 105 cells). Viral replication was monitored at the indicated days by measuring Gag-p24 production in culture supernatants. (B) HIV-exposed DCs promote efficient viral replication in HS clones. imDCs were exposed to HIVNL-AD8 (0.2 nM p24 for 106 cells), washed, and cocultured with HS L11 or N2 cells and with control 3.8 or 2.2 cells. Cells were grown in the absence of exogenous IL-2. As a control, the 4 clones were directly exposed to the same viral inputs and cultured without DCs, in the presence of IL-2. Two independent experiments are assembled: autologous DCs were used in the upper panels, and HLA-matched (HLA-DRβ*04+) DCs were used in the lower panels. Viral replication was monitored by measuring p24 production in culture supernatants. Data are representative of 4 independent experiments.

DCs promote infection of HS CD4+ cells. (A) Susceptibility of HS and control CD4+ clones to HIV replication. As a positive control for viral replication, 2 HS clones (L11 and N2) and 2 control clones with other antigenic specificities (3.8, 2.2) were activated with PHA and grown with IL-2. Cells were infected at a high moi (2 nM p24 for 3 × 105 cells). Viral replication was monitored at the indicated days by measuring Gag-p24 production in culture supernatants. (B) HIV-exposed DCs promote efficient viral replication in HS clones. imDCs were exposed to HIVNL-AD8 (0.2 nM p24 for 106 cells), washed, and cocultured with HS L11 or N2 cells and with control 3.8 or 2.2 cells. Cells were grown in the absence of exogenous IL-2. As a control, the 4 clones were directly exposed to the same viral inputs and cultured without DCs, in the presence of IL-2. Two independent experiments are assembled: autologous DCs were used in the upper panels, and HLA-matched (HLA-DRβ*04+) DCs were used in the lower panels. Viral replication was monitored by measuring p24 production in culture supernatants. Data are representative of 4 independent experiments.

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