The involvement of NLRP3 inflammasome in herpes simplex virus infection and treatment

Herpes simplex virus (HSV) can cause life-threatening diseases such as herpes simplex keratitis and herpes simplex encephalitis, with considerable tissue damage resulting from viral replication. The immune response that is activated in response to infection to control viral replication may become exaggerated and contribute to this damage. An overactive inflammatory response could be controlled using immunomodulatory strategies, an ideal target for which may be the multiple pattern recognition receptors that are involved in the innate immune response to HSV, including Toll-like receptors, RIG-I-like receptors, nucleotide oligomerization domain like receptors and cGAS-STING. Here, we summarize the role of the NLRP3 inflammasome in HSV infection and discuss the potential mechanism and therapeutic strategies of targeting the NLRP3 inflammasome for HSV-related diseases. Plain language summary: HSV can cause life-threatening conditions such as herpes simplex keratitis and herpes simplex encephalitis. The immune response to suppress viral replication may be exaggerated, leading to tissue damage. This may damage may be limited by using immunomodulatory strategies. For example, multiple receptors are involved in the innate immune response to HSV, including NLRP3, which may be ideal targets for immunomodulation. This article reviews the role of the NLRP3 inflammasome in HSV infection and discusses the mechanisms and treatment strategies utilizing the NLRP3 inflammasome in HSV-related diseases. Inflammation caused by HSV infection can sometimes lead to life-threatening pathologies. Studies have shown that HSV-induced inflammatory responses rely on NLRP3 inflammasome. This article reviews the role of the NLRP3 inflammasome in HSV infection.