Fig. 2: Enzymatic activity of AGPATs is required for HCV replication.

a Effect of AGPAT KO on HCV replication. Huh7.5 cells were infected with lentiviruses encoding AGPAT-targeting-sgRNAs and 5 days later, infected with an HCV reporter virus (JcR2a). After 48 h and 72 h, renilla luciferase activities in cell lysates, reflecting viral RNA replication, were quantified. Graph shows average and SD from three independent experiments. Significance was calculated by one-tailed paired t-test. p values are shown in graph. Abundance of AGPAT proteins is shown on the bottom. α-tubulin served as loading control. b Enzymatic activity of AGPAT is required for HCV replication. KO cells were reconstituted with sgRNA-resistant AGPAT wild-type (wt) or catalytically inactive mutants (M1 and M2) by lentiviral transduction. Cells were infected with JcR2a, and renilla luciferase activities were quantified. Graph shows average and SD from four independent experiments. Significance was calculated by one-tailed paired t-test. p values are shown in graph. Note the complete rescue by AGPAT1 and 2 co-expression. Abundance of AGPAT proteins is shown below the graph; α-tubulin served as loading control. c AGPAT1/2 DKO does not affect DENV or ZIKV propagation. Cells were infected with DENV-2 (strain 16681) or ZIKV (strain H/PF/2013) and 48 h later virus titer was quantified by plaque assay. Graph shows the average and SD from three independent experiments. Significance was analyzed by one-tailed paired t-test. p values are shown in graph. PFU, plaque-forming units. Source data for panels a, b and c are provided as Source Data file.