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Herpes simplex virus (HSV) infects eyes and causes herpetic stromal keratitis (HSK), a chronic inflammatory disease with excessive neovascularization in corneas. HSK has been the most common cause of corneal blindness in the western world due to infection. Host factors mediate HSK development, but little is known about these cellular factors and their mechanisms. A cell clone of rat intestine epithelial cells with mutation in annexin A1 (Anx-A1) gene is shown to be resistant to HSV-1 infection with unknown mechanisms. To date, the functions of Anx-A1 in HSK remain unclear. In the present study, we used a mouse model to investigate the roles of Anx-A1 in HSK. In vitro studies showed that Anx-A1 expression was enhanced after HSV-1 infection in mouse embryonic fibroblasts. In addition, the amount of virus produced by mouse embryonic fibroblasts cultured from Anx-A1-deficient mice was significantly lower than that produced by mouse embryonic fibroblasts from wild-type mice. Moreover, less mouse embryonic fibroblasts cultured from Anx-A1- deficient mice were infected by HSV-1 compared to those cultured from wild-type mice. In vivo studies demonstrated that the severity of HSK and viral load in the eyes of Anx-A1-deficient mice were significantly reduced compared with those of wild-type mice. Collectively, our results show that Anx-A1 aggravates HSK in mice.