Cargando…

Study of the host specificity of PB1-F2-associated virulence

Influenza A viruses cause important diseases in both human and animal. The PB1-F2 protein is a virulence factor expressed by some influenza viruses. Its deleterious action for the infected host is mostly described in mammals, while the available information is scarce in avian hosts. In this work, we...

Descripción completa

Detalles Bibliográficos
Autores principales: Mettier, Joëlle, Marc, Daniel, Sedano, Laura, Da Costa, Bruno, Chevalier, Christophe, Le Goffic, Ronan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8205076/
https://www.ncbi.nlm.nih.gov/pubmed/34125653
http://dx.doi.org/10.1080/21505594.2021.1933848
_version_ 1783708437020934144
author Mettier, Joëlle
Marc, Daniel
Sedano, Laura
Da Costa, Bruno
Chevalier, Christophe
Le Goffic, Ronan
author_facet Mettier, Joëlle
Marc, Daniel
Sedano, Laura
Da Costa, Bruno
Chevalier, Christophe
Le Goffic, Ronan
author_sort Mettier, Joëlle
collection PubMed
description Influenza A viruses cause important diseases in both human and animal. The PB1-F2 protein is a virulence factor expressed by some influenza viruses. Its deleterious action for the infected host is mostly described in mammals, while the available information is scarce in avian hosts. In this work, we compared the effects of PB1-F2 in avian and mammalian hosts by taking advantage of the zoonotic capabilities of an avian H7N1 virus. In vitro, the H7N1 virus did not behave differently when PB1-F2 was deficient while a H3N2 virus devoid of PB1-F2 was clearly less inflammatory. Likewise, when performing in vivo challenges of either chickens or embryonated eggs, with the wild-type or the PB1-F2 deficient virus, no difference could be observed in terms of mortality, host response or tropism. PB1-F2 therefore does not appear to play a major role as a virulence factor in the avian host. However, when infecting NF-κB-luciferase reporter mice with the H7N1 viruses, a massive PB1-F2-dependent inflammation was quantified, highlighting the host specificity of PB1-F2 virulence. Surprisingly, a chimeric 7:1 H3N2 virus harboring an H7N1-origin segment 2 (i.e. expressing the avian PB1-F2) induced a milder inflammatory response than its PB1-F2-deficient counterpart. This result shows that the pro-inflammatory activity of PB1-F2 is governed by complex mechanisms involving components from both the virus and its infected host. Thus, a mere exchange of segment 2 between strains is not sufficient to transmit the deleterious character of PB1-F2.
format Online
Article
Text
id pubmed-8205076
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Taylor & Francis
record_format MEDLINE/PubMed
spelling pubmed-82050762021-06-24 Study of the host specificity of PB1-F2-associated virulence Mettier, Joëlle Marc, Daniel Sedano, Laura Da Costa, Bruno Chevalier, Christophe Le Goffic, Ronan Virulence Research Paper Influenza A viruses cause important diseases in both human and animal. The PB1-F2 protein is a virulence factor expressed by some influenza viruses. Its deleterious action for the infected host is mostly described in mammals, while the available information is scarce in avian hosts. In this work, we compared the effects of PB1-F2 in avian and mammalian hosts by taking advantage of the zoonotic capabilities of an avian H7N1 virus. In vitro, the H7N1 virus did not behave differently when PB1-F2 was deficient while a H3N2 virus devoid of PB1-F2 was clearly less inflammatory. Likewise, when performing in vivo challenges of either chickens or embryonated eggs, with the wild-type or the PB1-F2 deficient virus, no difference could be observed in terms of mortality, host response or tropism. PB1-F2 therefore does not appear to play a major role as a virulence factor in the avian host. However, when infecting NF-κB-luciferase reporter mice with the H7N1 viruses, a massive PB1-F2-dependent inflammation was quantified, highlighting the host specificity of PB1-F2 virulence. Surprisingly, a chimeric 7:1 H3N2 virus harboring an H7N1-origin segment 2 (i.e. expressing the avian PB1-F2) induced a milder inflammatory response than its PB1-F2-deficient counterpart. This result shows that the pro-inflammatory activity of PB1-F2 is governed by complex mechanisms involving components from both the virus and its infected host. Thus, a mere exchange of segment 2 between strains is not sufficient to transmit the deleterious character of PB1-F2. Taylor & Francis 2021-06-14 /pmc/articles/PMC8205076/ /pubmed/34125653 http://dx.doi.org/10.1080/21505594.2021.1933848 Text en © 2021 Informa UK Limited, trading as Taylor & Francis Group https://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/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Mettier, Joëlle
Marc, Daniel
Sedano, Laura
Da Costa, Bruno
Chevalier, Christophe
Le Goffic, Ronan
Study of the host specificity of PB1-F2-associated virulence
title Study of the host specificity of PB1-F2-associated virulence
title_full Study of the host specificity of PB1-F2-associated virulence
title_fullStr Study of the host specificity of PB1-F2-associated virulence
title_full_unstemmed Study of the host specificity of PB1-F2-associated virulence
title_short Study of the host specificity of PB1-F2-associated virulence
title_sort study of the host specificity of pb1-f2-associated virulence
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8205076/
https://www.ncbi.nlm.nih.gov/pubmed/34125653
http://dx.doi.org/10.1080/21505594.2021.1933848
work_keys_str_mv AT mettierjoelle studyofthehostspecificityofpb1f2associatedvirulence
AT marcdaniel studyofthehostspecificityofpb1f2associatedvirulence
AT sedanolaura studyofthehostspecificityofpb1f2associatedvirulence
AT dacostabruno studyofthehostspecificityofpb1f2associatedvirulence
AT chevalierchristophe studyofthehostspecificityofpb1f2associatedvirulence
AT legofficronan studyofthehostspecificityofpb1f2associatedvirulence