Innate immune evasion mechanisms of filoviruses

Christopher F. Basler, Gaya K. Amarasinghe, Daisy W. Leung

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

The filoviruses, which include ebolaviruses (EBOVs) and marburgviruses (MARVs), are noteworthy because they cause severe, often deadly, hemorrhagic fever in humans. A central feature of filovirus biology is the ability to antagonize innate antiviral defenses of the host. This capacity likely contributes to uncontrolled virus replication and the severity of filoviral disease. This chapter reviews our current understanding of the ways in which filoviruses counter host innate antiviral defenses. Among the mechanisms discussed are VP35 proteins which inhibit several features of the innate immune response to infection, including RIG-I-like receptor signaling pathways that typically trigger interferon (IFN) production. The viruses also block the ability of infected cells to respond to IFNs. The EBOV VP24 protein inhibits nuclear translocation of the STAT1 transcription factor that is critical for IFN-induced gene expression. In MARVs, the VP40 protein blocks IFN-induced activation of the kinase Jak1, which normally phosphorylates and activates STAT1. In addition, these viruses are able to counteract the antiviral function of the IFN-induced protein tetherin, to modulate viral polymerase expression in response to cell stress and to avoid activating apoptosis. Understanding these immune evasion functions provides insights into the severity of filovirus disease and suggests new therapeutic approaches.

Original languageEnglish
Title of host publicationBiology and Pathogenesis of Rhabdo- and Filoviruses
PublisherWorld Scientific Publishing Co.
Pages557-586
Number of pages30
ISBN (Electronic)9789814635349
ISBN (Print)9789814635332
DOIs
StatePublished - Jan 1 2014

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