Fig. 4
From: HIV-1 with gag processing defects activates cGAS sensing

ISG induction by HIV-1 Gag-fusion virus is dependent on cGAS and STING. A: IFIT-1 reporter activity from monocytic THP-1-IFIT-1 cells lacking STING or MAVS, or a gRNA control (Ctrl) cell line transduced for 24 h with WT LAI or Gag-LUC (1.5 U RT/ml). B, C: ISG qPCR from monocytic THP-1-IFIT-1 cells lacking STING or MAVS, or a gRNA control (Ctrl) cell line transduced for 24 h with WT LAI or Gag-LUC (1.5 U RT/ml). D: IRF reporter activity from monocytic THP-1 Dual cells lacking cGAS, or a gRNA control (Ctrl) cell line transduced for 24 h with WT LAI or Gag-LUC (1.5 U RT/ml). E, F: ISG qPCR from monocytic THP-1 Dual cells lacking cGAS, or a gRNA control (Ctrl) cell line transduced for 24 h with WT LAI or Gag-LUC (1.5 U RT/ml). G: IRF reporter activity from monocytic THP-1 Dual cells lacking cGAS, or a gRNA control (Ctrl) cell line transduced for 24 h with WT LAI or Gag-LUC (1.5 U RT/ml), or stimulated by transfection with 0.05 µg/ml HT-DNA in the presence of DMSO vehicle, 0.5 µg/ml STING inhibitor H151 or 10 µg/ml cGAS inhibitor RU.521. Data are mean ± SD from biological triplicates of a single experiment, representative of at least 3 repeats. Statistical analyses were performed using Student’s t-test, with Welch’s correction where appropriate, comparing to Ctrl cells (A-F), or to DMSO vehicle treated cells (G) as indicated. *P < 0.05, **P < 0.01, ***P < 0.001, n.s. non-significant