Immune cell response process triggered by pattern recognition receptors signal in response to HSV-1

Inducing the secretion of inflammatory cytokines or interferon (IFN) through the Toll-like receptor (TLR) signaling pathway (left, middle) or the IG-I-like receptor (RLR) signaling pathway (right). In the TLR signaling pathway, TLR2 recognizes signals induced by HSV-1 envelope proteins, such as gB or gD. The signal is transmitted to the cytoplasm, where MyD88 binds to the cytoplasmic domain of TLR2, leading to the activation of transcription factors like NF-kappaB. This activation promotes the translocation of P50/P65 into the nucleus and increases the expression of inflammatory cytokines and IFN-1. Additionally, TLR3, TLR7/8, and TLR9 signaling are activated by dsRNA, ssRNA, or CpG DNA, respectively, in endosomes. These signals activate IRF-3, IRF-7, and NF-kappaB, ultimately resulting in increased expression in endosomes and increased inflammatory cytokines, IFN-1, IFN-III, and interferon-stimulated genes (ISGs). In the RLR signaling pathway, RIG-I and MDA5, which contain N-terminal caspase activation and recruitment domains, recruit and activate the mitochondrial antiviral signaling (MAVS) protein to mediate signal transduction. The activated MAVS protein further activates downstream signaling, promoting the expression of inflammatory cytokines and IFN. Both pathways contribute to the immune response against HSV-1 infection by triggering the production of inflammatory cytokines and interferons, which play crucial roles in controlling viral replication and coordinating innate and adaptive immune responses. (Source: Zhao Z, Liu X, Zong Y, Shi X, Sun Y. Cellular processes induced by HSV-1 infections in vestibular neuritis. Viruses 2023;16[1]:12. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)