We speculate that these GP1 N-terminal cleavages are normally mediated by the sequential activity of endosomal cysteine aminopeptidases such as CatC or CatH but can be more promiscuously carried out by cysteine endoproteases like CatL in the context of the A82V mutation, thereby contributing to the observed enhancements in viral entry and infection. Here, CTSL is linked to infection.