Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

    We have a manual that explains all the features 

Record number 505739
Title Alphavirus infection : Host cell shut-off and inhibition of antiviral responses
Author(s) Fros, Jelke J.; Pijlman, Gorben P.
Source Viruses 8 (2016)6. - ISSN 1999-4915
DOI http://dx.doi.org/10.3390/v8060166
Department(s) Laboratory of Virology
PE&RC
Publication type Refereed Article in a scientific journal
Publication year 2016
Keyword(s) Alphavirus - Antiviral response - Chikungunya - Host shut-off - Interferon - Semliki forest - Sindbis - Stress granules - Transcription - Translation - Unfolded protein response
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.

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