The Involvement of NLRP3 Inflammasome in Herpes Simplex Virus Infection and Treatment

Abstract

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.

Tweetable abstract

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.

Keywords::

• encephalitis
• HSV
• keratitis
• NLRP3
• STING
• virulence

Author contributions

Y Ding and HF Yu wrote the manuscript. LQ Ding conceived the work and revised the manuscript. All authors read and approved the final manuscript.

Financial & competing interests disclosure

This work was supported by the Scientific Research Project of the Education Department of Hubei Province (Q20212805) and the Initial Scientific Research Fund of PhDs in Hubei University of Science and Technology (BK202120). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by the Scientific Research Project of the Education Department of Hubei Province (Q20212805) and the Initial Scientific Research Fund of PhDs in Hubei University of Science and Technology (BK202120). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.