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Figure 1.

Effects of macrophage-tropic HIV-1 strain and VSV-G-pseudotyped HIV-2 particles on lentivirus vector infection.

Monocytes were differentiated into macrophages for 11 days in the presence of GM-CSF. Macrophages or monocytes were treated with macrophage-tropic HIV-1 strain (SF162) or VSV-G pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G) and then infected with lentivirus vector NL43-Luci/VSV-G. Luciferase activity was measured 4 days after infection. Data are plotted as the mean ± SD of triplicate samples; presented data are representative of three independent experiments using two donors. A: Results of samples obtained from a donor 1. B: Results of samples obtained from a donor 2.

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Figure 2.

Effects of VSV-G-pseudotyped HIV-2 particles on macrophage-tropic and T-cell line-tropic HIV-1 strains in GM-CSF-induced macrophages.

Monocytes were differentiated into macrophages for 6 days in the presence of GM-CSF. Macrophages were treated with VSV-G pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G) and then infected with HIV-1 strain SF162 or NL43. HIV-1 replication was quantified by ELISA measurement of p24 antigen in the supernatant after infection. Data are plotted as the mean ± SD of triplicate samples; presented data are representative of three independent experiments using two donors. A: Results of samples obtained from a donor 1. B: Results of samples obtained from a donor 2.

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Figure 2 Expand

Figure 3.

Effects of VSV-G-pseudotyped HIV-2 particles on macrophage-tropic and T-cell line-tropic HIV-1 strains in M-CSF-induced macrophages.

Monocytes were differentiated into macrophages for 6 days in the presence of M-CSF. Macrophages were treated with VSV-G pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G) and then infected with HIV-1 strain SF162 or NL43. HIV-1 replication was quantified by ELISA measurement of p24 antigen in the supernatant after infection. Data are plotted as the mean ± SD of triplicate samples; presented data are representative of two independent experiments using two donors. A: Results of samples obtained from a donor 1. B: Results of samples obtained from a donor 2.

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Figure 3 Expand

Figure 4.

Effects of VSV-G-pseudotyped HIV-2 particles on macrophage-tropic and T-cell line-tropic HIV-1 strains in undifferentiated monocytes.

Monocytes were treated with VSV-G pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G) and then infected with HIV-1 strain SF162 or NL43. HIV-1 replication was quantified by ELISA measurement of p24 antigen in the supernatant after infection. Data are plotted as the mean ± SD of triplicate samples obtained from a single blood donor; presented data are representative of three independent experiments using two donors. A: Results of samples obtained from a donor 1. B: Results of samples obtained from a donor 2.

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Figure 5.

Syncytium formation in undifferentiated monocytes pretreated with HIV-2 particles and then infected with macrophage-tropic HIV-1.

Monocytes were treated with VSV-G pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G) and then infected with HIV-1 strain SF162 or NL43. Presented data are representative of two independent experiments.

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Figure 5 Expand

Figure 6.

Western blot analysis of SAMHD1 in undifferentiated monocytes and macrophages.

Monocytes were differentiated into macrophages for 6 days in the presence of GM-CSF or M-CSF. Macrophages or monocytes were treated with or without VSV-G-pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G), and harvested. Whole-cell extracts were separated on SDS-PAGE and analyzed by western blot using the indicated antibodies. Presented data are representative of two independent experiments.

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Figure 7.

Quantification of SAMHD1 mRNA expression.

Monocytes were differentiated into macrophages for 6 days in the presence of GM-CSF or M-CSF. Macrophages or monocytes were treated with or without VSV-G-pseudotyped and Env-defective HIV-2 particles (GH123/VSV-G), and harvested. SAMHD1 mRNA expression levels were detected by real-time RT-PCR and normalized against GAPDH. Data are shown as mean ± SD.

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Figure 8.

Phosphorylation state of SAMHD1.

Monocytes (Monocyte), M-CSF-differentiated macrophages (Macrophage (M-CSF)), and GM-CSF-differentiated macrophages (Macrophage (GM-CSF)) were treated with GH123-Nhe/VSV-G for 2 h and incubated at 37°C for 4 h (4 h) or 24 h (24 h), or mock-treated (−). Cells were lyzed and subjected for SDS-PAGE containing Phos-tag to separate phosphorylated proteins from nonphosphorylated ones. SAMHD1 proteins were detected by anti-SAMHD1 antibody. Upper bands shown by a vertical bar and a lower band shown by an arrow represent phosphorylated and nonphosphorylated SAMHD1, respectively. Ratios of phosphorylated SAMHD1 levels to total SAMHD1 levels (ratio) are shown in vertical numbers.

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Figure 9.

Effects of SAMHD1 siRNA on HIV-1 infection.

Monocytes (Monocyte) or macrophages (Macrophage) were treated with SAMHD1- (siSAMHD1) or GFP- (siGFP) targeting siRNAs. Three days after transfection, cells were harvested or infected with NL43-Luci/VSV-G virus. SAMHD1 mRNA expression levels in harvested cells were detected by real-time RT-PCR and normalized against GAPDH. Data are shown as mean ± SD. Luciferase activity in infected cells was measured 4 days after infection. Data are plotted as the mean ± SD of triplicate samples; presented data are representative of two independent experiments using two donors. A: Results of samples obtained from a donor 1. B: Results of samples obtained from a donor 2.

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