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. 2021 Mar 26;17(3):e1009446. doi: 10.1371/journal.ppat.1009446

Fig 8. The γ134.5-RIG-I interaction influences HSV-1 replication.

Fig 8

(A) Viral replication in Rig-I+/+ or Rig-I-/- MEFs. Cells were infected with wild-type HSV-1 or the γ134.5 deletion virus (Δγ134.5) at a MOI 0.01. At 48 h postinfection, virus yields were determined on Vero cells by plaque assay. (B) Kinetics of viral growth in Rig-I+/+ or Rig-I-/- MEFs. Viral infection was performed as described for panel (A) and viral yields were measured at the indicated time points. (C) Viral replication in control and RIG-I knockdown human lung fibroblasts cells. shCtrl (control) or shRIG-I (RIG-I knockdown) HEL cells were infected with wild type HSV-1 or Δγ134.5 (0.01 pfu/cell). At 48 h postinfection, virus yields were determined by plaque assay. (D) Kinetics of viral growth in control and RIG-I knockdown cells. Viral infection was performed as described in panel (C) and viral yields were measured at the indicated time points. The data are representative of results from three experiments with triplicate samples. Differences between the selected groups were statistically assessed by one-way ANOVA (A and C) or a two-tailed Student’s t test (B and D) (**, P < 0.01).