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Updated: Feb 26, 2026

Analysis of Group IV Viral SSHHPS Using In Vitro and In Silico Methods
Published on: December 21, 2019
Schlafen 14 (SLFN14) is a novel antiviral factor involved in the control of viral replication
Rak-Kyun Seong1, Seong-Wook Seo1, Ji-Ae Kim1
1Department of Biomedical Sciences, College of Medicine, Korea University, Seoul, Republic of Korea.
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-β 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.
Insights
Schlafen 14 (SLFN14) acts as a novel antiviral factor. This protein inhibits viral replication for both RNA and DNA viruses by impacting viral translocation and enhancing immune signaling.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Schlafen (SLFN) proteins are implicated in cell proliferation and immune cell development.
- The antiviral functions of SLFN14, an RNA-helicase domain-containing protein, were investigated.
Purpose of the Study:
- To determine the antiviral activities of SLFN14 against viral infections.
- To elucidate the mechanisms by which SLFN14 exerts its antiviral effects.
Main Methods:
- Murine SLFN14 expression was analyzed in RAW264.7 macrophages induced by TLR3 and type I interferon (IFN).
- Cells were infected with influenza viruses (PR8 and delNS1/PR8) to study SLFN14 induction.
- SLFN14's effect on viral replication was assessed via overexpression in A549 cells and knockdown in RAW264.7 cells.
- Viral NP translocation and RIG-I-mediated IFN-β signaling were evaluated.
Main Results:
- SLFN14 expression was induced by TLR3-mediated pathways, type I IFN, and influenza virus infection.
- SLFN14 overexpression reduced influenza virus replication, while SLFN14 knockdown enhanced viral titers.
- SLFN14 delayed viral NP translocation and boosted RIG-I-mediated IFN-β signaling.
- SLFN14 also demonstrated antiviral activity against varicella zoster virus (VZV), a DNA virus.
Conclusions:
- SLFN14 is a novel antiviral factor effective against both RNA and DNA viruses.
- SLFN14 functions by inhibiting viral replication, delaying nuclear translocation, and enhancing innate immune responses.
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