Figure 2

Platelets inhibit HIV-1 spread in T cells and release an anti-HIV-1 activity upon activation. (A) PHA stimulated PBMCs were infected with 10 pg of HIV-1 NL4-3 in the presence of untreated platelets (PLT, 1 × 10⁸/mL) or medium alone (control) and p24-antigen content in the supernatants was measured on day one and six post infection. The p24-antigen levels at day one post infection were below detection range. The results of a single representative experiment performed in duplicates are shown, error bars indicate SD. The results were confirmed in an independent experiment. (B) Platelets inhibit HIV-1 spread in adjacent T cells in a concentration- and activation status- dependent manner. The indicated amounts of non-resting platelets (PLT, platelets left untreated) or activated platelets (A-PLT, platelets treated with TRAP) were added to C8166-SEAP T cells, the cultures infected with 10 pg of HIV-1 NL4-3 and SEAP-activity measured at day five post infection. The average ± SEM of three experiments performed in triplicates is shown, SEAP-activity measured in the absence of platelets was set as 100%. (C) Activation of platelets induces the release of one or more HIV-1 inhibitory factors. The indicator cell line TZM-bl was incubated with supernatants from resting (R-PLT Sup) and activated platelets (A-PLT Sup) or incubated with PBS or PBS containing 10 μM PGE₁ or 100 μM TRAP. Subsequently, the cells were infected with HIV-1 NL4-3 and luciferase activities in the lysates of infected cells were measured. The results ± SD of a single experiment performed in triplicates is shown. Similar results were obtained in a separate experiment.