Although PLA2G16 knockout reduces the permissiveness of H1-HeLa cells for enterovirus infection (Staring et al., 2017), longer term studies demonstrated that the replication of both HAV and eHAV was enhanced in ΔPLA2G16 cells, with increased hepatovirus RNA abundance, more dsRNA, and greater viral protein synthesis (Figure 5B-Figure 5—figure supplement 1A,B). This evidence concerns the gene PLAAT3 and enterovirus infectious disease.