HDAC6 and infection: On the contrary, HIV-1 early infection was enhanced with viruses produced in HEK 293T cells overexpressing HDAC6-ΔBUZ, where Vif level was increased and A3G apparently protected from Vif degradation (Figure 10b, histograms, bars in lanes 5 and 6), suggesting that HDAC6-ΔBUZ competes with the anti-HIV-1 activity of the endogenous HDAC6, thus controlling Vif expression level and infectiveness (Figure 10b, compare Vif and infection between lane 2 and lanes 5–6).