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

Bruno Hernáez, Juan Manuel Alonso-Lobo, Imma Montanuy, Cornelius Fischer, Sascha Sauer, Luis Sigal, Noemí Sevilla and Antonio Alcamí ()
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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
Sascha Sauer: Max Planck Institute for Molecular Genetics
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)

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-07772-z

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