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A virus-encoded type I interferon decoy receptor enables evasion of host immunity through cell-surface binding

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  • Bruno Hernáez

    (Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM))

  • Juan Manuel Alonso-Lobo

    (Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM))

  • Imma Montanuy

    (Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM))

  • Cornelius Fischer

    (Max Planck Institute for Molecular Genetics
    Max Delbrück Center for Molecular Medicine (BIMSB/BIH))

  • Sascha Sauer

    (Max Planck Institute for Molecular Genetics
    Max Delbrück Center for Molecular Medicine (BIMSB/BIH))

  • Luis Sigal

    (Thomas Jefferson University)

  • Noemí Sevilla

    (Centro de Investigación en Sanidad Animal; Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria)

  • Antonio Alcamí

    (Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM))

Abstract

Soluble cytokine decoy receptors are potent immune modulatory reagents with therapeutic applications. Some virus-encoded secreted cytokine receptors interact with glycosaminoglycans expressed at the cell surface, but the biological significance of this activity in vivo is poorly understood. Here, we show the type I interferon binding protein (IFNα/βBP) encoded by vaccinia and ectromelia viruses requires of this cell binding activity to confer full virulence to these viruses and to retain immunomodulatory activity. Expression of a variant form of the IFNα/βBP that inhibits IFN activity, but does not interact with cell surface glycosaminoglycans, results in highly attenuated viruses with a virulence similar to that of the IFNα/βBP deletion mutant viruses. Transcriptomics analysis and infection of IFN receptor-deficient mice confirmed that the control of IFN activity is the main function of the IFNα/βBP in vivo. We propose that retention of secreted cytokine receptors at the cell surface may largely enhance their immunomodulatory activity.

Suggested Citation

  • Bruno Hernáez & Juan Manuel Alonso-Lobo & Imma Montanuy & Cornelius Fischer & Sascha Sauer & Luis Sigal & Noemí Sevilla & Antonio Alcamí, 2018. "A virus-encoded type I interferon decoy receptor enables evasion of host immunity through cell-surface binding," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07772-z
    DOI: 10.1038/s41467-018-07772-z
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    Cited by:

    1. Carina Jacobsen & Nina Plückebaum & George Ssebyatika & Sarah Beyer & Lucas Mendes-Monteiro & Jiayi Wang & Kai A. Kropp & Víctor González-Motos & Lars Steinbrück & Birgit Ritter & Claudio Rodríguez-Go, 2024. "Viral modulation of type II interferon increases T cell adhesion and virus spread," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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