Figure 4.
Figure 4. Tat enhances HIV-1 entry and spreading. (A) Tat enhances entry of both CXCR4-dependent HIV-1 strain III B and CCR5-dependent HIV-1 strain Ba-L. PBMCs were either untreated (▦) or pretreated with rTat (▪) and immediately infected with either III B or Ba-L. Virus entry was evaluated by a densitometric analysis of the amount of early viral transcripts in the cytoplasm. Tat-mediated increases of III B and Ba-L entry were semiquantitatively corrected by the cognate GAPDH values and expressed as percent of respective control infections. (B) Tat enhances virus spreading in vitro. The amount of HIV-1 produced by infected cells was measured as RT activity in culture supernatants (F = 165.1; *P ≤ .005 within rTat-treated and control cells). ○ indicates treatment with rTat; ▪, control. Similar results were obtained with III B HIV-1 strain. Each value indicates mean ± SD of 3 experiments performed in duplicate.

Tat enhances HIV-1 entry and spreading. (A) Tat enhances entry of both CXCR4-dependent HIV-1 strain III B and CCR5-dependent HIV-1 strain Ba-L. PBMCs were either untreated (▦) or pretreated with rTat (▪) and immediately infected with either III B or Ba-L. Virus entry was evaluated by a densitometric analysis of the amount of early viral transcripts in the cytoplasm. Tat-mediated increases of III B and Ba-L entry were semiquantitatively corrected by the cognate GAPDH values and expressed as percent of respective control infections. (B) Tat enhances virus spreading in vitro. The amount of HIV-1 produced by infected cells was measured as RT activity in culture supernatants (F = 165.1; *P ≤ .005 within rTat-treated and control cells). ○ indicates treatment with rTat; ▪, control. Similar results were obtained with III B HIV-1 strain. Each value indicates mean ± SD of 3 experiments performed in duplicate.

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