Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.

Murid γ-herpesvirus-4 (MuHV-4) promotes polyclonal B cell activation and establishes latency in memory B cells via unclear mechanisms. We aimed at exploring whether B cell receptor specificity plays a role in B cell susceptibility to viral latency and how this is related to B cell activation. We fir...

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Autores principales:	Jérémie Decalf, Cristina Godinho-Silva, Diana Fontinha, Sofia Marques, J Pedro Simas
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/4e3b2de0548047eba4664407440290d4
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spelling	oai:doaj.org-article:4e3b2de0548047eba4664407440290d42021-11-25T05:46:13ZEstablishment of murine gammaherpesvirus latency in B cells is not a stochastic event.1553-73661553-737410.1371/journal.ppat.1004269https://doaj.org/article/4e3b2de0548047eba4664407440290d42014-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25079788/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Murid γ-herpesvirus-4 (MuHV-4) promotes polyclonal B cell activation and establishes latency in memory B cells via unclear mechanisms. We aimed at exploring whether B cell receptor specificity plays a role in B cell susceptibility to viral latency and how this is related to B cell activation. We first observed that MuHV-4-specific B cells represent a minority of the latent population, and to better understand the influence of the virus on non-MuHV-4 specific B cells we used the SWHEL mouse model, which produce hen egg lysozyme (HEL)-specific B cells. By tracking HEL+ and HEL- B cells, we showed that in vivo latency was restricted to HEL- B cells while the two populations were equally sensitive to the virus in vitro. Moreover, MuHV-4 induced two waves of B cell activation. While the first wave was characterized by a general B cell activation, as shown by HEL+ and HEL- B cells expansion and upregulation of CD69 expression, the second wave was restricted to the HEL- population, which acquired germinal center (GC) and plasma cell phenotypes. Antigenic stimulation of HEL+ B cells led to the development of HEL+ GC B cells where latent infection remained undetectable, indicating that MuHV-4 does not benefit from acute B cell responses to establish latency in non-virus specific B cells but relies on other mechanisms of the humoral response. These data support a model in which the establishment of latency in B cells by γ-herpesviruses is not stochastic in terms of BCR specificity and is tightly linked to the formation of GCs.Jérémie DecalfCristina Godinho-SilvaDiana FontinhaSofia MarquesJ Pedro SimasPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 7, p e1004269 (2014)
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 Jérémie Decalf Cristina Godinho-Silva Diana Fontinha Sofia Marques J Pedro Simas Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
description	Murid γ-herpesvirus-4 (MuHV-4) promotes polyclonal B cell activation and establishes latency in memory B cells via unclear mechanisms. We aimed at exploring whether B cell receptor specificity plays a role in B cell susceptibility to viral latency and how this is related to B cell activation. We first observed that MuHV-4-specific B cells represent a minority of the latent population, and to better understand the influence of the virus on non-MuHV-4 specific B cells we used the SWHEL mouse model, which produce hen egg lysozyme (HEL)-specific B cells. By tracking HEL+ and HEL- B cells, we showed that in vivo latency was restricted to HEL- B cells while the two populations were equally sensitive to the virus in vitro. Moreover, MuHV-4 induced two waves of B cell activation. While the first wave was characterized by a general B cell activation, as shown by HEL+ and HEL- B cells expansion and upregulation of CD69 expression, the second wave was restricted to the HEL- population, which acquired germinal center (GC) and plasma cell phenotypes. Antigenic stimulation of HEL+ B cells led to the development of HEL+ GC B cells where latent infection remained undetectable, indicating that MuHV-4 does not benefit from acute B cell responses to establish latency in non-virus specific B cells but relies on other mechanisms of the humoral response. These data support a model in which the establishment of latency in B cells by γ-herpesviruses is not stochastic in terms of BCR specificity and is tightly linked to the formation of GCs.
format	article
author	Jérémie Decalf Cristina Godinho-Silva Diana Fontinha Sofia Marques J Pedro Simas
author_facet	Jérémie Decalf Cristina Godinho-Silva Diana Fontinha Sofia Marques J Pedro Simas
author_sort	Jérémie Decalf
title	Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
title_short	Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
title_full	Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
title_fullStr	Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
title_full_unstemmed	Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.
title_sort	establishment of murine gammaherpesvirus latency in b cells is not a stochastic event.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/4e3b2de0548047eba4664407440290d4
work_keys_str_mv	AT jeremiedecalf establishmentofmurinegammaherpesviruslatencyinbcellsisnotastochasticevent AT cristinagodinhosilva establishmentofmurinegammaherpesviruslatencyinbcellsisnotastochasticevent AT dianafontinha establishmentofmurinegammaherpesviruslatencyinbcellsisnotastochasticevent AT sofiamarques establishmentofmurinegammaherpesviruslatencyinbcellsisnotastochasticevent AT jpedrosimas establishmentofmurinegammaherpesviruslatencyinbcellsisnotastochasticevent
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Establishment of murine gammaherpesvirus latency in B cells is not a stochastic event.

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