HSV-1 infection promotes the ubiquitination and degradation of KEAP1-dependent Nrf2, leading to reduced expression of downstream anti-iron deposition genes, disrupting cellular redox homeostasis, and promoting iron accumulation.HSV-1-induced ferroptosis activates the upregulation of PTGS2 and PGE2, promoting the development of encephalitis. This evidence concerns the gene NFE2L2 and viral encephalitis.