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. 2020 Aug 27;39(20):e103958. doi: 10.15252/embj.2019103958

Figure EV3. Innate immune activation is RT‐dependent.

Figure EV3

  1. Infection data from Fig 3A and B. THP-1‐IFIT-1 cells transduced for 48 h with HIV‐1 GFP containing 0% (WT) or 75% ΔCA‐SP1 mutant (1 U RT/ml) in the presence of DMSO vehicle, 5 μM nevirapine or 10 μM raltegravir.
  2. Infection data for Fig 3C and D. THP-1‐IFIT-1 cells transduced for 48 h with 0% (WT) or 75% ΔCA‐SP1 mutant (109 and 3 × 109 genomes/ml) in the presence of DMSO vehicle, 5 μM nevirapine or 10 μM raltegravir.
  3. Infection data for Fig 3E and F. THP-1‐IFIT-1 cells transduced for 48 h with HIV‐1 GFP containing 0% ΔCA‐SP1 (WT), 75% ΔCA‐SP1, 75% ΔCA‐SP1 carrying a mutation in reverse transcriptase (75% ΔCA‐SP1 RT D185E) or 75% ΔCA‐SP1 carrying a mutation in integrase (75% ΔCA‐SP1 INT D116N) (3.75 × 109, 7.5 × 109 and 1.5 × 1010 genomes/ml).
  4. Infection data for PMA‐treated THP‐1 Dual shSAMHD1 cells transduced for 48 h with 75% ΔCA‐SP1, 75% ΔCA‐SP1 RT D185E or 75% ΔCA‐SP1 INT D116N (3 × 109 genomes/ml).
  5. Infection data for PMA‐treated THP‐1 Dual shSAMHD1 control cells transduced for 48 h with WT HIV‐1 GFP or 90% ΔCA‐SP1 mutant (1 × 1010 genomes/ml) in the presence of DMSO vehicle, 5 μM nevirapine or 10 μM raltegravir.
Data information: Data are mean ± SD, n = 3, representative of 2 repeats.