Fig 1.

Stat1, Irf1 Atg5, Atg16l1, and Gate-16 are required for IFNγ-induced inhibition of norovirus replication in BV-2 cells, Atg14, Becn1, and Uvrag are not; GATE-16 is required for IFNγ-induced growth restriction of T. gondii in HeLa cells. (A) Plaque assay of WT, Irf1^−/−, and Stat1^−/− BV-2 cells as described in Fig. S1. (B) Viability assay of WT, Irf1^−/−, and Stat1^−/− BV-2 cells as described in Fig. S1. (C–E) Plaque assay of WT, Atg5^−/−, Ag16l1^−/−, Atg14^−/−, Becn1^−/−, Uvrag^−/−, and Atg8 family members in BV-2 cells. (F) WT, ATG16L1^−/−, and GATE16^−/− were treated with IFNγ and infected with T. gondii. Parasites within ubiquitin-positive (+) and ubiquitin-negative (−) vacuoles were counted by immunofluorescence microscopy. Average data pooled from 2 to 3 independent experiments are represented as means ± standard error of the mean (SEM). *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, and ****P ≤ 0.0001 were considered statistically significant. ns, not significant. P value was determined by two-way analysis of variance (ANOVA) with Dunnett’s multiple comparison test; for T. gondii assay, P value was determined by two-way ANOVA with Tukey’s multiple comparison test.