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. 2009 Aug 3;106(33):14046–14051. doi: 10.1073/pnas.0907344106

Fig. 5.

Fig. 5.

Autophagy machinery does not regulate established HCV replication. (A) Replicon bearing-Huh-7 cells were transduced with lentiviral vectors expressing shRNAs against Beclin-1, Atg4B, and GFP. Protein and RNA levels were determined 10 days posttransduction. (Upper Left) NS5A protein levels in replicon cells as analyzed by immunoblotting. (Upper Right) Intracellular HCV RNA levels in H77 (1a), con-1 (1b), JFH-1 (2a) SGR, or JFH-1 full-length (FLR) replicon-bearing Huh-7 cells monitored by RT-qPCR (mean ± SD; n = 2). GE, genome equivalent. (Lower) Efficiency of down-regulation of Beclin-1, Atg4B, as analyzed by immunoblotting. Beclin-1 and Atg4B content were analyzed in established JFH-1 SGR replicon cells (denoted Replicon cells) and were compared to shRNA-treated cells before HCV infection (denoted DR before infection). β-actin expression was used as a protein loading control. (B) Huh-7 cells that were virtually all infected by HCV were transduced with lentiviral vectors expressing shRNA against Beclin-1, Atg4B. (Left) Relative levels of Beclin-1 and Atg4B in the infected cells, as analyzed by immunoblotting. β-actin expression was used as a protein loading control. (Right) Extracellular and intracellular infectivity and intracellular HCV RNA levels were determined 8 days posttransduction and are expressed as a percentage of those in control cells (mean ± SD; n = 2).