Interferons during HSV-2 Infection: Immune Regulation

Abstract

Herpes simplex virus type 2 (HSV-2) infection is a prevalent sexually transmitted infection that disproportionately affects women worldwide. Currently, there are no vaccines or curative treatments available, leading to life-long infections. During HSV-2 infection, interferons (IFNs) play a crucial role in the body's antiviral defense. Type I IFNs (IFN-alpha and IFN-beta) and type III IFNs (IFN-lambda) are produced by host cells in response to the virus, alerting neighboring cells to its presence and inducing an antiviral state that limits viral replication and spread. Type III IFNs, produced in epithelial cells, also contribute to controlling viral replication in mucosal tissues. However, HSV-2 has evolved strategies to evade IFN-induced responses, allowing the virus to partially escape the host's immune response, establish latency, and cause recurrent infections. The delicate balance between the host's IFN response and the virus's immune evasion mechanisms determines the outcome of HSV-2 infection. Understanding the intricate interplay between HSV-2 and interferon signalling is critical for developing effective therapies and vaccines to combat this sexually transmitted infection. Keywords: HSV-2, Interferons, Innate immunity, Immune regulation