PKR activation elicits a stronger antiviral response than MAVS-mediated IFN induction.

(A) Growth curve analyses of MeV-vac2(GFP) in HeLa, ADAR1KO (clone E7), ADAR1KO-MAVSKO (clones F2 and F4), and ADAR1KO-PKRKO cells (clones H3 and HI3) infected at an MOI of 0.1 and harvested at indicated time points. Values are average ± standard deviation of n = 6 for each time point. P values were determined by unpaired, two-tailed Student’s t test (*, P ≤ 0.05; **, P ≤ 0.001; ***, P ≤ 0.0001). Underlying values can be found in S1 Data. (B) Western blot analysis of cell lysates of UI or MeV-CKO(GFP)-infected cells at an MOI of 3, 24 h post infection. (C) Quantification of the pIRF3(S386) signals (top panel) and pPKR(T446) signals (bottom panel) shown in (B). Values are average ± standard deviation of two independent experiments. Underlying values can be found in S1 Data. ADAR1, adenosine deaminase acting on RNA 1; ADAR1KO, fully ADAR1-deficient; FL-MAVS, full-length MAVS; IFN, interferon; IRF3, IFN regulatory transcription factor 3; MAVS, mitochondrial antiviral signaling protein; MeV, measles virus; MOI, multiplicity of infection; N, nucleoprotein; p150KO, selectively ADAR1p150-deficient; pIRF3, phospho-IRF3; PKR, protein kinase R; pPKR, phospho-PKR; UI, uninfected.