Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses
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...
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| Format: | Online |
| Language: | English |
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MDPI
2016
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926186/ |
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pubmed-4926186 |
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pubmed-49261862016-07-06 Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses Fros, Jelke J. Pijlman, Gorben P. Review 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. MDPI 2016-06-11 /pmc/articles/PMC4926186/ /pubmed/27294951 http://dx.doi.org/10.3390/v8060166 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/). |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Fros, Jelke J. Pijlman, Gorben P. |
| spellingShingle |
Fros, Jelke J. Pijlman, Gorben P. Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| author_facet |
Fros, Jelke J. Pijlman, Gorben P. |
| author_sort |
Fros, Jelke J. |
| title |
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| title_short |
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| title_full |
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| title_fullStr |
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| title_full_unstemmed |
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses |
| title_sort |
alphavirus infection: host cell shut-off and inhibition of antiviral responses |
| description |
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. |
| publisher |
MDPI |
| publishDate |
2016 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926186/ |
| _version_ |
1613601330499158016 |