Lambda-Interferons Inhibit Herpes Simplex Virus Type 2 Replication in Human Cervical Epithelial Cells by Activating the JAK/STAT Pathway
作者： Zhu Li , Xuan Lu , Yufan Zhu , Pengfei Cheng , Shi Liu
DOI: 10.7883/YOKEN.JJID.2016.465
关键词: Receptor 、 JAK-STAT signaling pathway 、 stat 、 Janus kinase 、 Cancer research 、 Signal transduction 、 Herpes simplex virus 、 Virology 、 Transcription (biology) 、 Biology 、 Pattern recognition receptor
摘要: Herpes simplex virus type 2 (HSV-2) is associated with a variety of diseases that are health problems worldwide. Our early study showed lambda-interferons (IFN-λs), induced by the activation Toll-like receptor 3 and retinoic acid-inducible protein I signaling pathways, contribute to inhibition HSV-2 replication in human cervical epithelial cells. However, anti-HSV-2 mechanisms specific differences transduction different IFN-λs cells remain unclear. In this study, we demonstrated potent without cytotoxicity. Investigation underlying mechanism(s) expression IFN-stimulated genes (ISGs) enhanced several pattern recognition receptors (PRRs). Among IFN-λs, IFN-λ3 higher levels ISG PRR expression. addition, up-regulated number encode components Janus kinase signal transducers activators transcription (JAK/STAT) pathway. Inhibition JAK/STAT pathway JAK inhibitor abolished IFN-λ-mediated activity induction ISGs PRRs, whereas PRRs was not compromised infection. These findings provide further experimental evidence have therapeutic potential for infections.
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