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Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2
Superinfection exclusion (SIE) is a process by which a virally infected cell is protected from subsequent infection by the same or a closely related virus. By preventing cell coinfection, SIE favors preservation of genome integrity of a viral strain and limits its recombination potential with other...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7660575/ https://www.ncbi.nlm.nih.gov/pubmed/33180795 http://dx.doi.org/10.1371/journal.pone.0241592 |
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author | Boussier, Jeremy Levi, Laura Weger-Lucarelli, James Poirier, Enzo Z. Vignuzzi, Marco Albert, Matthew L. |
author_facet | Boussier, Jeremy Levi, Laura Weger-Lucarelli, James Poirier, Enzo Z. Vignuzzi, Marco Albert, Matthew L. |
author_sort | Boussier, Jeremy |
collection | PubMed |
description | Superinfection exclusion (SIE) is a process by which a virally infected cell is protected from subsequent infection by the same or a closely related virus. By preventing cell coinfection, SIE favors preservation of genome integrity of a viral strain and limits its recombination potential with other viral genomes, thereby impacting viral evolution. Although described in virtually all viral families, the precise step(s) impacted by SIE during the viral life cycle have not been systematically explored. Here, we describe for the first time SIE triggered by chikungunya virus (CHIKV), an alphavirus of public health importance. Using single-cell technologies, we demonstrate that CHIKV excludes subsequent infection with: CHIKV; Sindbis virus, a related alphavirus; and influenza A, an unrelated RNA virus. We further demonstrate that SIE does not depend on the action of type I interferon, nor does it rely on host cell transcription. Moreover, exclusion is not mediated by the action of a single CHIKV protein; in particular, we observed no role for non-structural protein 2 (nsP2), making CHIKV unique among characterized alphaviruses. By stepping through the viral life cycle, we show that CHIKV exclusion occurs at the level of replication, but does not directly influence virus binding, nor viral structural protein translation. In sum, we characterized co-infection during CHIKV replication, which likely influences the rate of viral diversification and evolution. |
format | Online Article Text |
id | pubmed-7660575 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-76605752020-11-18 Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 Boussier, Jeremy Levi, Laura Weger-Lucarelli, James Poirier, Enzo Z. Vignuzzi, Marco Albert, Matthew L. PLoS One Research Article Superinfection exclusion (SIE) is a process by which a virally infected cell is protected from subsequent infection by the same or a closely related virus. By preventing cell coinfection, SIE favors preservation of genome integrity of a viral strain and limits its recombination potential with other viral genomes, thereby impacting viral evolution. Although described in virtually all viral families, the precise step(s) impacted by SIE during the viral life cycle have not been systematically explored. Here, we describe for the first time SIE triggered by chikungunya virus (CHIKV), an alphavirus of public health importance. Using single-cell technologies, we demonstrate that CHIKV excludes subsequent infection with: CHIKV; Sindbis virus, a related alphavirus; and influenza A, an unrelated RNA virus. We further demonstrate that SIE does not depend on the action of type I interferon, nor does it rely on host cell transcription. Moreover, exclusion is not mediated by the action of a single CHIKV protein; in particular, we observed no role for non-structural protein 2 (nsP2), making CHIKV unique among characterized alphaviruses. By stepping through the viral life cycle, we show that CHIKV exclusion occurs at the level of replication, but does not directly influence virus binding, nor viral structural protein translation. In sum, we characterized co-infection during CHIKV replication, which likely influences the rate of viral diversification and evolution. Public Library of Science 2020-11-12 /pmc/articles/PMC7660575/ /pubmed/33180795 http://dx.doi.org/10.1371/journal.pone.0241592 Text en © 2020 Boussier et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Boussier, Jeremy Levi, Laura Weger-Lucarelli, James Poirier, Enzo Z. Vignuzzi, Marco Albert, Matthew L. Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title | Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title_full | Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title_fullStr | Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title_full_unstemmed | Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title_short | Chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
title_sort | chikungunya virus superinfection exclusion is mediated by a block in viral replication and does not rely on non-structural protein 2 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7660575/ https://www.ncbi.nlm.nih.gov/pubmed/33180795 http://dx.doi.org/10.1371/journal.pone.0241592 |
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