Figure 1
Figure 1. VLPs inhibit HIV-1 replication. (A-B) PHA-stimulated PBMCs were infected with (A) X4 virus (HIV-1NL4.3) or (B) R5 virus (HIV-1Ad8) as described in “Materials and methods.” The infected cells were cultured for 7 days in the presence of various concentrations of VLPs. (C) PHA-stimulated PBMCs were infected with X4 virus for 2 hours and then cultured for 7 days in the absence or the presence of 1 μg/mL baculovirus extract or VLPs. (D) PHA-stimulated PBMCs were infected with X4 virus for 2 hours and then cultured for 7 days in the absence or the presence of 1 μg/mL VLPs, SV40-VLPs, or BVLPs. In all experiments, half of the culture supernatants was changed on the 4th day with fresh culture media alone. HIV-1 replication was measured by p24 antigen capture assay. Data show means ± SDs and are representative of at least 3 independent experiments.

VLPs inhibit HIV-1 replication. (A-B) PHA-stimulated PBMCs were infected with (A) X4 virus (HIV-1NL4.3) or (B) R5 virus (HIV-1Ad8) as described in “Materials and methods.” The infected cells were cultured for 7 days in the presence of various concentrations of VLPs. (C) PHA-stimulated PBMCs were infected with X4 virus for 2 hours and then cultured for 7 days in the absence or the presence of 1 μg/mL baculovirus extract or VLPs. (D) PHA-stimulated PBMCs were infected with X4 virus for 2 hours and then cultured for 7 days in the absence or the presence of 1 μg/mL VLPs, SV40-VLPs, or BVLPs. In all experiments, half of the culture supernatants was changed on the 4th day with fresh culture media alone. HIV-1 replication was measured by p24 antigen capture assay. Data show means ± SDs and are representative of at least 3 independent experiments.

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