Figure S1.
IFITM3 reduces PV infectivity at the level of producer and target cell for IAV and HIV-1 but not for VSV in an HIV-1–based PV system. (a and b) A549 cells (a) or TZM-bl cells (b) were infected for 48 h with the indicated PVs produced in the absence of IFITM3. Luciferase expression obtained after infection with PVno env was set to 1 and used to normalize luciferase values. Mean values from at least three independent replicates are shown with error bars representing SD. (c) Schematic depiction of PVIAV produced in the absence or presence of IFITM3 and the cell lines, which were control transduced or transduced to stably express IFITM3. (d) A549 control cells or A549-IFITM3 cells were infected for 48 h with PVIAV produced in the absence or presence IFITM3. Luciferase activity was measured and infectivity calculated by setting values obtained for A549 control cells infected with PVIAV produced in the absence of IFITM3 to 100%. (e) TZM-bl control cells or TZM-bl-IFITM3 cells were infected for 48 h with PVHIV produced in the absence or presence IFITM3. Luciferase activity was measured and infectivity calculated by setting values obtained for TZM-bl control cells infected with PVHIV produced in the absence of IFITM3 to 100%. (f) TZM-bl control cells or TZM-bl-IFITM3 cells were infected for 48 h with PVVSV produced in the absence or presence of IFITM3. Luciferase activity was measured and infectivity calculated by setting values obtained for TZM-bl control cells infected with PVVSV produced in the absence of IFITM3 to 100%. (d–f) Mean values from three biological replicates, each performed in triplicates, are shown with error bars representing SD. Statistical significance was assessed by a paired two-tailed Student’s t test (*, P < 0.05; **, P < 0.01), comparing infectivity in the different conditions with infectivity of PVs produced in the absence of IFITMs on IFITM3-negative cells.