Figure 6
Figure 6. HIC CD4 T-cell resistance is overcome by increasing viral inoculum or cell-to-cell transmission. (A) HIV-1 BaL replication on day 7 after infection in anti–CD3-activated CD4+ T cells from one representative HIC (top) and the logarithmic fold reduction in viral replication compared with cells infected in parallel from a HD (bottom) in various experimental conditions. Cells were challenged as follows: in suboptimal conditions (first column), with a higher cell density (106 cells/mL; second column), using a spinoculation protocol to facilitate viral binding to the cell surface (third column), and using both a higher cell density and spinoculation (fourth column). Means ± SDs are shown (in the bottom panel, standard deviations are relative to the mean infection level measured in cells from HDs). (B) Levels of p24 in culture supernatants of CD4+ T cells from one HIC (circles) and one HD (triangles) at day 9 after infection in suboptimal conditions with serial dilutions of HIV-1 BaL.

HIC CD4 T-cell resistance is overcome by increasing viral inoculum or cell-to-cell transmission. (A) HIV-1 BaL replication on day 7 after infection in anti–CD3-activated CD4+ T cells from one representative HIC (top) and the logarithmic fold reduction in viral replication compared with cells infected in parallel from a HD (bottom) in various experimental conditions. Cells were challenged as follows: in suboptimal conditions (first column), with a higher cell density (106 cells/mL; second column), using a spinoculation protocol to facilitate viral binding to the cell surface (third column), and using both a higher cell density and spinoculation (fourth column). Means ± SDs are shown (in the bottom panel, standard deviations are relative to the mean infection level measured in cells from HDs). (B) Levels of p24 in culture supernatants of CD4+ T cells from one HIC (circles) and one HD (triangles) at day 9 after infection in suboptimal conditions with serial dilutions of HIV-1 BaL.

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