IFNL1 and infection: This hypothesis is supported by the clustered spatial distribution of HCV-infected cells noted herein, and previously described by Wieland et al. in liver biopsies obtained from chronically HCV-infected patients.[43] Furthermore, the level of IFN-λ-1 released in HCV-infected iHLC cultures is sufficient to inhibit de novo infection in naive hepatocytes.[19] In patients, endogenous IFN-λs may therefore induce an environment within uninfected hepatocytes that is refractory to further stimulation by alfa, which may thus impact treatment outcome.