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Nat Commun. 2018 Sep 6;9(1):3603. doi: 10.1038/s41467-018-06000-y.

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

Author information

1
Department of Microbiology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, 75390, TX, USA.
2
Department of Microbiology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, 75390, TX, USA. john.schoggins@utsouthwestern.edu.

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.

PMID:
30190477
PMCID:
PMC6127192
DOI:
10.1038/s41467-018-06000-y
[Indexed for MEDLINE]
Free PMC Article

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