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LY6E mediates an evolutionarily conserved enhancement of virus infection by targeting a late entry step

Author

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  • Katrina B. Mar

    (University of Texas Southwestern Medical Center)

  • Nicholas R. Rinkenberger

    (University of Texas Southwestern Medical Center)

  • Ian N. Boys

    (University of Texas Southwestern Medical Center)

  • Jennifer L. Eitson

    (University of Texas Southwestern Medical Center)

  • Matthew B. McDougal

    (University of Texas Southwestern Medical Center)

  • R. Blake Richardson

    (University of Texas Southwestern Medical Center)

  • John W. Schoggins

    (University of Texas Southwestern Medical Center)

Abstract

Interferons (IFNs) contribute to cell-intrinsic antiviral immunity by inducing hundreds of interferon-stimulated genes (ISGs). In a screen to identify antiviral ISGs, we unexpectedly found that LY6E, a member of the LY6/uPAR family, enhanced viral infection. Here, we show that viral enhancement by ectopically expressed LY6E extends to several cellular backgrounds and affects multiple RNA viruses. LY6E does not impair IFN antiviral activity or signaling, but rather promotes viral entry. Using influenza A virus as a model, we narrow the enhancing effect of LY6E to uncoating after endosomal escape. Diverse mammalian orthologs of LY6E also enhance viral infectivity, indicating evolutionary conservation of function. By structure-function analyses, we identify a single amino acid in a predicted loop region that is essential for viral enhancement. Our study suggests that LY6E belongs to a class of IFN-inducible host factors that enhance viral infectivity without suppressing IFN antiviral activity.

Suggested Citation

  • Katrina B. Mar & Nicholas R. Rinkenberger & Ian N. Boys & Jennifer L. Eitson & Matthew B. McDougal & R. Blake Richardson & John W. Schoggins, 2018. "LY6E mediates an evolutionarily conserved enhancement of virus infection by targeting a late entry step," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06000-y
    DOI: 10.1038/s41467-018-06000-y
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    Cited by:

    1. Xinyu Xie & Pin Wang & Min Jin & Yue Wang & Lijie Qi & Changhua Wu & Shu Guo & Changqing Li & Xiaojun Zhang & Ye Yuan & Xinyi Ma & Fangying Liu & Weiyuan Liu & Heng Liu & Chen Duan & Ping Ye & Xuezhon, 2024. "IL-1β-induced epithelial cell and fibroblast transdifferentiation promotes neutrophil recruitment in chronic rhinosinusitis with nasal polyps," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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