Upon infection with the DNA virus herpes simplex virus type 1 (HSV-1), the stimulator of interferon genes (STING) binds to NLRP3, attenuates K48- and K63-linked ubiquitination of NLRP3 and increases its protein expression on the endoplasmic reticulum, facilitating NLRP3 inflammasome activation and the subsequent release of proinflammatory cytokines [44]. This evidence concerns the gene NLRP3 and infection.