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. Author manuscript; available in PMC: 2015 Jun 24.
Published in final edited form as: Gastroenterology. 2014 Jan 31;146(5):1351–60.e1-4. doi: 10.1053/j.gastro.2014.01.054

Figure 4. HCV activates the PKR-eIF2α pathway, and PKR-silencing restores MHC class I expression.

Figure 4

(A) Huh-7.5 cells were infected with HCVcc at 0.1 MOI and cultured for 3 days, with an infection rate of 85–95%. HCV-infected or uninfected cells were treated with 3 ng/mL IFN-β or 10 ng/mL IFN-γ for 24 h, and cell lysates were analyzed by immunoblotting. (B) PKR-silenced stable cell lines were established by PKR shRNA-lentivirus transduction. Complete (shPKR#4) or partial (shPKR#1) silencing of PKR expression was confirmed by immunoblotting. The density of the immunoblot bands was quantified and presented in the graph on the bottom. (C and D) PKR-silenced or unsilenced Huh-7.5 cells were inoculated with HCV at 0.01 MOI, cultured for 3 days (yielding an infection rate of 30–45%) and treated with 3 ng/mL IFN-β. The expression level of MHC class I in HCV-infected (blue) or uninfected (red) cells was analyzed by co-staining for HCV core and MHC class I and flow cytometry (C). Expression of MHC class I was compared between HCV core-positive and -negative cells (D). Data represent mean + SEM of three independent experiments. **, P < 0.01; ***, P < 0.001; ns, not significant.