Schlafen 14 (SLFN14) is a novel antiviral factor involved in the control of viral replication

Research output: Contribution to journalArticle

Authors

  • Rak-Kyun Seong
  • Seong-Wook Seo
  • Ji-Ae Kim
  • Mukesh Kumar
  • Young-Ki Choi
  • Ok Sarah Shin

Colleges, School and Institutes

External organisations

  • Department of Biomedical Sciences, College of Medicine, Korea University
  • Department of Tropical Medicine, Medical Microbiology and Pharmacology, Pacific Center for Emerging Infectious Diseases Research, John A. Burns School of Medicine, University of Hawaii at Manoa
  • College of Medicine and Medical Research Institute, Chungbuk National University

Abstract

Schlafen (SLFN) proteins have been suggested to play important functions in cell
proliferation and immune cell development. In this study, we determined the antiviral activities of putative RNA-helicase domain-containing SLFN14. Murine SLFN14 expression was specifically induced by TLR3-mediated pathways and type I interferon (IFN) in RAW264.7 mouse macrophages. To examine the role of SLFN during viral infection, cells were infected with either wild-type PR8 or delNS1/PR8 virus. SLFN14 expression was specifically induced following influenza virus infection. Overexpression of SLFN14 in A549 cells reduced viral replication, whereas knockdown of SLFN14 in RAW264.7 cells enhanced
viral titers. Furthermore, SLFN14 promoted the delay in viral NP translocation from cytoplasm to nucleus and enhanced RIG-I-mediated IFN-signaling. In addition, SLFN14 overexpression promoted antiviral activity against varicella zoster virus (VZV), a DNA virus. In conclusion, our data suggest that SLFN14 is a novel antiviral factor for both DNA and RNA viruses.

Details

Original languageEnglish
JournalImmunobiology
Early online date11 Jul 2017
Publication statusE-pub ahead of print - 11 Jul 2017

Keywords

  • SLFN14 , influenza, VZV , interferon, anti-viral