Journal: PLoS Pathogens
Article Title: The herpesvirus accessory protein γ 1 34.5 facilitates viral replication by disabling mitochondrial translocation of RIG-I
doi: 10.1371/journal.ppat.1009446
Figure Lengend Snippet: (A) Viral replication in Rig-I +/+ or Rig-I -/- MEFs. Cells were infected with wild-type HSV-1 or the γ 1 34.5 deletion virus (Δγ 1 34.5) 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 Δγ 1 34.5 (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).
Article Snippet: Vero, HEK-293T, Human lung embryonic (HEL) fibroblasts cells were obtained from the American Type Culture Collection.
Techniques: Infection, Virus, Plaque Assay, Control, Knockdown, Two Tailed Test