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Lambda-Interferons Inhibit Herpes Simplex Virus Type 2 Replication in Human Cervical Epithelial Cells by Activating the JAK/STAT Pathway

Lambda-Interferons Inhibit Herpes Simplex Virus Type 2 Replication in Human Cervical Epithelial Cells by Activating the JAK/STAT Pathway

Zhu Li, Xuan Lu, Yufan Zhu, Pengfei Cheng, Shi Liu, Yi Zhang, Jingfeng Tang, Sijun Yang, Li Zhou

Jpn J Infect Dis. 2017 Jul 24;70(4):416-422.

PMID: 28250263

Abstract:

Herpes simplex virus type 2 (HSV-2) is associated with a variety of diseases that are health problems worldwide. Our early study showed that lambda-interferons (IFN-λs), induced by the activation of the Toll-like receptor 3 and retinoic acid-inducible protein I signaling pathways, contribute to inhibition of HSV-2 replication in human cervical epithelial cells. However, anti-HSV-2 mechanisms and specific differences in signaling transduction by different IFN-λs in human cervical epithelial cells remain unclear. In this study, we demonstrated potent inhibition of HSV-2 replication by IFN-λs without cytotoxicity. Investigation of the underlying mechanism(s) showed that IFN-λs induced expression of IFN-stimulated genes (ISGs) and enhanced the expression of several pattern recognition receptors (PRRs). Among the IFN-λs, IFN-λ3 induced higher levels of ISG and PRR expression. In addition, IFN-λs up-regulated a number of genes that encode components of the Janus kinase signal transducers and activators of transcription (JAK/STAT) signaling pathway. Inhibition of the JAK/STAT signaling pathway by a JAK inhibitor abolished IFN-λ-mediated anti-HSV-2 activity and induction of ISGs and PRRs, whereas the induction of ISGs and PRRs by IFN-λs was not compromised by HSV-2 infection. These findings provide further experimental evidence that IFN-λs have therapeutic potential for HSV-2 infections.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413321	IFN-lambda 2 human			Price

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