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Fe 2+ overload, ROS accumulation, GSH depletion, LPO, and mitochondrion shrinkage were observed in HSV-1-infected cultured human astrocytes, microglia and murine brains, which are hallmarks of ferroptosis ( HSV-1 infection enhanced the ubiquitination and degradation of Nrf2 mediated by Kelch-like ECH-related protein 1 (Keap1) so as to inhibit the expression of antioxidative genes, which disturbed cellular redox homeostasis and promoted ferroptosis (Gunderstofte et al., 2019)

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