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PLoS One. 2014 Apr 10;9(4):e94806. doi: 10.1371/journal.pone.0094806. eCollection 2014.

HSV-2 increases TLR4-dependent phosphorylated IRFs and IFN-β induction in cervical epithelial cells.

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  • 1State Key Laboratory of Virology, Institute of Medical Virology, Wuhan University School of Medicine, Wuhan, Hubei, China; Shengzhen R&D Center of State Key Laboratory of Virology, Wuhan University Shenzhen Institute, Shenzhen, Guangdong, China.
  • 2Central Blood Station of Rizhao, Rizhao, Shandong, China.


Our previous studies demonstrated that HSV-2 infection up-regulates TLR4 expression and induces NF-kB activity, thereby facilitating innate immune response in human cervical epithelial cells. This process requires involvement of TLR4 adaptors, Mal and MyD88. In the current study, we found that HSV-2 infection increases levels of phosphoryalted IRF3 and IRF7, then regulating expression of type I IFN. As expected, these changes induced by HSV-2 infection depended upon TLR4. Knockdown of TRIF and/or TRAM by siRNAs indicated that TRIF/TRAM might be involved in expression of IFN-β. Our results demonstrate for the first time that IRF3 and IRF7 are both involved in inducing TLR4-dependent IFN-β expression in response to HSV-2 in its primary infected genital epithelial cells. Thus, TLR4-Mal/MyD88 and TLR4-TRIF/TRAM signaling may synergize and/or cooperate in innate immune response of cervical epithelial cells to HSV-2 infection.

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