Figure 5
From: Efficient BST2 antagonism by Vpu is critical for early HIV-1 dissemination in humanized mice
Effect of Vpu mutated in the β-TrCP-binding domain on the dynamics of HIV infection in hu-mice. Hu-mice were infected with high dose of HIV-1-WT, HIV-1-∆Vpu, or HIV-1-VpuD52/56 and plasma viral load was determined at different time points. (A) shows kinetics of RNA copy number per ml of plasma (log10) and (B) shows absolute values at 21-dpi in plasma of hu-mice infected with the indicated HIV-1. Please note that x-axis crosses at log10 value of 3.0. (C) shows comparison of the frequency of p24+ T cells in spleen of hu-mice infected with the indicated HIV-1 (n ≥ 7) at 21-dpi. (D) shows type I IFN levels at 21-dpi in plasma of hu-mice infected with the indicated HIV-1. (E) shows impact of Vpu mutations on BST2 and CD4 levels on p24+ and p24- T cells from individual hu-mouse infected with the indicated strain of HIV-1. (F) shows comparison of relative BST2 and CD4 levels on p24+ (closed bar) and p24- (open bar) T cells from spleen of hu-mice infected with the indicated strain of HIV-1 at 21-dpi (n ≥ 4). BST2 and CD4 MFIs on p24-negative uninfected cells were treated as 100%. Error bars represent SD; *, p ≤ 0.05; **, p ≤ 0.005, ***, p ≤ 0.0005, N.S.: non significant.