cbVGs induce translation inhibition in SG-positive cells.

(A) SG (G3BP1 white) and viral protein (SeV NP) detection in control and MAVS KO A549 cells 24 hpi with SeV cbVG-high virus at MOI 1.5 TCID50/cell 24 hpi. CTCF quantification of SeV viral protein NP in control and MAVS KO A549 SG-positive cells. (B) G3BP1 (green) for SG detection and PMY (magenta) for translation in cells infected with SeV cbVG-high (SeV NP, red) at MOI 3 TCID50/cell 24 hpi or treated with sodium arsenite, with and without treatment with PMY for 5 min. (C) Quantification of PMY intensity (CTCF) in cells after drug treatment with sodium arsenite or SG-positive and SG-negative SeV cbVG-high infected cells. Each dot represents the CTCF average of approximately 100 cells counted for each condition. Widefield images were acquired with the Apotome 2.0 at 63× magnification, scale bar = 50 μm. Statistical analysis: one-way ANOVA (*p D) Diagram summarizing the role cbVGs have in inducing virus interference through activation of MAVS signaling and induction of translation inhibition. Numerical values plotted can be found in the Supporting information: S1 Data. cbVG, copy-back viral genome; CTCF, corrected total cell fluorescence; G3BP1, GTPase-activating protein-binding protein 1; hpi, hours postinfection; KO, knockout; MAVS, mitochondrial antiviral signaling; MOI, multiplicity of infection; NP, nucleoprotein; PMY, puromycin; SeV, Sendai virus; SG, stress granule.