This antiviral phenotype is suggested by the gradual increase from NK1 to NK3 of Granzyme H, which destroys critical adenoviral viral proteins that inhibit granzyme B, which is also present in NK3.190 Granzyme H also destroys the La-mediated HCV-IRES translational activity.191 Similarly, the exclusive expression of CCL5 in NK3 suggests antiviral defenses against Influenza A virus.192 Moreover, IL-32, which is elevated in NK3, plays a crucial role in responding to infections caused by viruses like HIV-1 and influenza. This evidence concerns the gene GZMH and influenza.