Alphavirus infection: Host cell shut-off and inhibition of antiviral responses

Jelke J. Fros, Gorben P. Pijlman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

38 Citations (Scopus)

Abstract

Alphaviruses cause debilitating disease in humans and animals and are transmitted by blood-feeding arthropods, typically mosquitoes. With a traditional focus on two models, Sindbis virus and Semliki Forest virus, alphavirus research has significantly intensified in the last decade partly due to the re-emergence and dramatic expansion of chikungunya virus in Asia, Europe, and the Americas. As a consequence, alphavirus–host interactions are now understood in much more molecular detail, and important novel mechanisms have been elucidated. It has become clear that alphaviruses not only cause a general host shut-off in infected vertebrate cells, but also specifically suppress different host antiviral pathways using their viral nonstructural proteins, nsP2 and nsP3. Here we review the current state of the art of alphavirus host cell shut-off of viral transcription and translation, and describe recent insights in viral subversion of interferon induction and signaling, the unfolded protein response, and stress granule assembly.

Original languageEnglish
Article number166
JournalViruses
Volume8
Issue number6
DOIs
Publication statusPublished - 2016

Keywords

  • Alphavirus
  • Antiviral response
  • Chikungunya
  • Host shut-off
  • Interferon
  • Semliki forest
  • Sindbis
  • Stress granules
  • Transcription
  • Translation
  • Unfolded protein response

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