Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.

Marek's disease virus (MDV) is an alphaherpesvirus that causes immunosuppression and deadly lymphoma in chickens. Lymphoid organs play a central role in MDV infection in animals. B-cells in the bursa of Fabricius facilitate high levels of MDV replication and contribute to dissemination at early...

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Autores principales:	Laëtitia Trapp-Fragnet, Julia Schermuly, Marina Kohn, Luca D Bertzbach, Florian Pfaff, Caroline Denesvre, Benedikt B Kaufer, Sonja Härtle
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/8a68d4424bbf46c2967747934bbdafb5
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spelling	oai:doaj.org-article:8a68d4424bbf46c2967747934bbdafb52021-12-02T19:59:59ZMarek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.1553-73661553-737410.1371/journal.ppat.1010006https://doaj.org/article/8a68d4424bbf46c2967747934bbdafb52021-10-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1010006https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Marek's disease virus (MDV) is an alphaherpesvirus that causes immunosuppression and deadly lymphoma in chickens. Lymphoid organs play a central role in MDV infection in animals. B-cells in the bursa of Fabricius facilitate high levels of MDV replication and contribute to dissemination at early stages of infection. Several studies investigated host responses in bursal tissue of MDV-infected chickens; however, the cellular responses specifically in bursal B-cells has never been investigated. We took advantage of our recently established in vitro infection system to decipher the cellular responses of bursal B-cells to infection with a very virulent MDV strain. Here, we demonstrate that MDV infection extends the survival of bursal B-cells in culture. Microarray analyses revealed that most cytokine/cytokine-receptor-, cell cycle- and apoptosis-associated genes are significantly down-regulated in these cells. Further functional assays validated these strong effects of MDV infections on cell cycle progression and thus, B-cell proliferation. In addition, we confirmed that MDV infections protect B-cells from apoptosis and trigger an accumulation of the autophagy marker Lc3-II. Taken together, our data indicate that MDV-infected bursal B-cells show hallmarks of a senescence-like phenotype, leading to a prolonged B-cell survival. This study provides an in-depth analysis of bursal B-cell responses to MDV infection and important insights into how the virus extends the survival of these cells.Laëtitia Trapp-FragnetJulia SchermulyMarina KohnLuca D BertzbachFlorian PfaffCaroline DenesvreBenedikt B KauferSonja HärtlePublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 17, Iss 10, p e1010006 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Laëtitia Trapp-Fragnet Julia Schermuly Marina Kohn Luca D Bertzbach Florian Pfaff Caroline Denesvre Benedikt B Kaufer Sonja Härtle Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
description	Marek's disease virus (MDV) is an alphaherpesvirus that causes immunosuppression and deadly lymphoma in chickens. Lymphoid organs play a central role in MDV infection in animals. B-cells in the bursa of Fabricius facilitate high levels of MDV replication and contribute to dissemination at early stages of infection. Several studies investigated host responses in bursal tissue of MDV-infected chickens; however, the cellular responses specifically in bursal B-cells has never been investigated. We took advantage of our recently established in vitro infection system to decipher the cellular responses of bursal B-cells to infection with a very virulent MDV strain. Here, we demonstrate that MDV infection extends the survival of bursal B-cells in culture. Microarray analyses revealed that most cytokine/cytokine-receptor-, cell cycle- and apoptosis-associated genes are significantly down-regulated in these cells. Further functional assays validated these strong effects of MDV infections on cell cycle progression and thus, B-cell proliferation. In addition, we confirmed that MDV infections protect B-cells from apoptosis and trigger an accumulation of the autophagy marker Lc3-II. Taken together, our data indicate that MDV-infected bursal B-cells show hallmarks of a senescence-like phenotype, leading to a prolonged B-cell survival. This study provides an in-depth analysis of bursal B-cell responses to MDV infection and important insights into how the virus extends the survival of these cells.
format	article
author	Laëtitia Trapp-Fragnet Julia Schermuly Marina Kohn Luca D Bertzbach Florian Pfaff Caroline Denesvre Benedikt B Kaufer Sonja Härtle
author_facet	Laëtitia Trapp-Fragnet Julia Schermuly Marina Kohn Luca D Bertzbach Florian Pfaff Caroline Denesvre Benedikt B Kaufer Sonja Härtle
author_sort	Laëtitia Trapp-Fragnet
title	Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
title_short	Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
title_full	Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
title_fullStr	Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
title_full_unstemmed	Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.
title_sort	marek's disease virus prolongs survival of primary chicken b-cells by inducing a senescence-like phenotype.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/8a68d4424bbf46c2967747934bbdafb5
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Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.

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