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. 2006 Oct 11;81(1):309–318. doi: 10.1128/JVI.01411-06

FIG. 3.

FIG. 3.

HCV RNA and HCV infection activate CXCL-8 transcription. (A) Huh7.5.1 cells were transfected with RIG-WT and the full-length −1481 CXCL-8 luciferase construct, and 24 h later, cells were mock transfected, transfected with JFH-1 RNA, or infected with Sendai virus (SeV) at 100 hemagglutinin inhibitor units. Luciferase readings were measured 24 h later. Asterisks indicate that JFH-1- or Sendai virus-induced CXCL-8 transcription was significantly higher than mock-transfected cells (*, P <0.01). RLU, relative light units. (B) Huh7.5.1 cells were transfected with RIG-WT and the full-length −1481 CXCL-8 luciferase construct, and 24 h later, cells were infected with JFH-1 virus stocks at an MOI of 0.01. Control cells were incubated with an equivalent volume of supernatants from cells transfected with replication-incompetent JFH-1 RNA containing the GND mutation in the viral polymerase. Luciferase readings were taken at the indicated times. Data are expressed as the increase (n-fold) in luciferase values over that of the GND control. (C) Western blot detection of HCV NS3, NS5A, and core proteins in Huh7.5.1 cells infected with JFH-1 at an MOI of 0.01. Blots were also probed with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) to verify equal protein loading.