Fig. 3
From: PIM kinases facilitate lentiviral evasion from SAMHD1 restriction via Vpx phosphorylation
Low infectivity of HIV-2 bearing Vpx-S13A in myeloid cells. a–d Single-cycle HIV-2 infection assays in various human macrophages. Schematic representation of the experimental design (a). Briefly, monocytic cells were differentiated into macrophages by PMA or M-CSF and then infected with the indicated HIV-2 encoding luciferase (Luc) reporter gene. Forty-eight hours after infection, intracellular luciferase activity was measured for Monomac6 (MM6) (b), U937 (c) and primary monocyte-derived macrophage (d). Endogenous SAMHD1 expression in infected cells is also shown. Bar charts below the blot indicate the ratio of SAMHD1 over Tubulin, as determined by densitometry. e, f Multi-cycle HIV-2 replication kinetics in THP1-derived macrophages. Schematic representation of the experimental procedure (e). Cells were infected with wild-type HIV-2GL-AN and its Vpx-S13A, Q76A, and Vpx-deficient mutants. RT activity of each supernatant was measured at the indicated time points (f). g SAMHD1 expression in the indicated HIV-2–infected THP1-macrophages, 12 days after infection. Bar chart below the blot indicates the ratio of SAMHD1 over Tubulin, as determined by densitometry.All graphs are presented as a mean ± s.d. (n = 3). *P < 0.05; **P < 0.01; ns, not significant, two-tailed unpaired t-test. Source data are provided as a Source Data file
