Surprisingly, infection of an LSD1 overexpressing cell line with HCV revealed a strong inhibition of viral propagation, despite a transient sharp peak in the rate of active HCV replication in the first 6 h p.i. This result hinted at a putative inhibiting role for LSD1 on HCV infection, which could explain the need for NS5A to mediate the down-regulation of endogenous LSD1 post endocytosis. Here, KDM1A is linked to infection.