For example, whileE418R that shows 60% reduced lipid uptake capacity induced wild-typeHDL-mediated infection-enhancement, the most disabled lipid transfer mutants,Q402R and Q402R-E418R, had lost almost all infection-enhancement capacity (Figure 5C and 5D).Collectively, the results demonstrated that SR-BI functions as an HCV entryfactor by providing both cell surface binding sites and lipid uptake activity. Here, SCARB1 is linked to infection.