Interestingly, we found that reconstitution of wild‐type TRPV1 but not TRPV1D646N/E648/651Q (which lost the Ca2+ permeability) into Lyz2‐Cre;Trpv2fl/fl BMDCs almost fully restored HSV‐1‐induced Ca2+ influx and the penetration and infection of HSV‐1, indicating an indispensable role of TRPV channels‐mediated Ca2+ influx for the entry of HSV‐1. Here, TRPV1 is linked to infection.