Apolipoprotein B100 is required for hepatitis C infectivity and Mipomersen inhibits hepatitis C

Figure 1 APOB genetic knockout Huh 7 hepatoma cells inefficiently support hepatitis C virus. A: Using TALEN genetic deletion of APOB, knockout huh7/CD81 (high) cells were generated (APOB^-/-, KO). We demonstrated that these cells inefficiently support hepatitis C virus (HCV) infection with the fully infectious tissue culture HCV virus, HCVcc (JFH1). There was markedly decreased JFH1 72 h following infection both at the level of HCV core protein and RNA. Data is shown as mean with 95% confidence interval, normalized to WT; B: To confirm this was not a clone-specific effect, three additional clones were infected with the JFH1 virus and intracellular HCV RNA assessed 72 h following infection. We again found a decrease in HCV RNA in the APOB KO clones (^aP < 0.05); C, D: Rescue experiments were performed by treating cells with human LDL at the same time as infection with the JFH1 virus. We found partial restoration of intracellular apoB expression at 72 h following exposure (D), and there was a partial restoration of HCV infection, with increased expression of HCV core protein (C), HCV RNA (E), and IF demonstrating increased HCV core expression in the LDL-treated cells (D). Scale bar: 20 μm.