Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.

Gamma-herpesviruses persist in lymphocytes and cause disease by driving their proliferation. Lymphocyte infection is therefore a key pathogenetic event. Murid Herpesvirus-4 (MuHV-4) is a rhadinovirus that like the related Kaposi's Sarcoma-associated Herpesvirus persists in B cells in vivo yet i...

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Autores principales:	Bruno Frederico, Ricardo Milho, Janet S May, Laurent Gillet, Philip G Stevenson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/78884973648844a49b0d65b544b96ed1
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spelling	oai:doaj.org-article:78884973648844a49b0d65b544b96ed12021-11-18T06:03:56ZMyeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.1553-73661553-737410.1371/journal.ppat.1002935https://doaj.org/article/78884973648844a49b0d65b544b96ed12012-09-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028329/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Gamma-herpesviruses persist in lymphocytes and cause disease by driving their proliferation. Lymphocyte infection is therefore a key pathogenetic event. Murid Herpesvirus-4 (MuHV-4) is a rhadinovirus that like the related Kaposi's Sarcoma-associated Herpesvirus persists in B cells in vivo yet infects them poorly in vitro. Here we used MuHV-4 to understand how virion tropism sets the path to lymphocyte colonization. Virions that were highly infectious in vivo showed a severe post-binding block to B cell infection. Host entry was accordingly an epithelial infection and B cell infection a secondary event. Macrophage infection by cell-free virions was also poor, but improved markedly when virion binding improved or when macrophages were co-cultured with infected fibroblasts. Under the same conditions B cell infection remained poor; it improved only when virions came from macrophages. This reflected better cell penetration and correlated with antigenic changes in the virion fusion complex. Macrophages were seen to contact acutely infected epithelial cells, and cre/lox-based virus tagging showed that almost all the virus recovered from lymphoid tissue had passed through lysM(+) and CD11c(+) myeloid cells. Thus MuHV-4 reached B cells in 3 distinct stages: incoming virions infected epithelial cells; infection then passed to myeloid cells; glycoprotein changes then allowed B cell infection. These data identify new complexity in rhadinovirus infection and potentially also new vulnerability to intervention.Bruno FredericoRicardo MilhoJanet S MayLaurent GilletPhilip G StevensonPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 8, Iss 9, p e1002935 (2012)
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 Bruno Frederico Ricardo Milho Janet S May Laurent Gillet Philip G Stevenson Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
description	Gamma-herpesviruses persist in lymphocytes and cause disease by driving their proliferation. Lymphocyte infection is therefore a key pathogenetic event. Murid Herpesvirus-4 (MuHV-4) is a rhadinovirus that like the related Kaposi's Sarcoma-associated Herpesvirus persists in B cells in vivo yet infects them poorly in vitro. Here we used MuHV-4 to understand how virion tropism sets the path to lymphocyte colonization. Virions that were highly infectious in vivo showed a severe post-binding block to B cell infection. Host entry was accordingly an epithelial infection and B cell infection a secondary event. Macrophage infection by cell-free virions was also poor, but improved markedly when virion binding improved or when macrophages were co-cultured with infected fibroblasts. Under the same conditions B cell infection remained poor; it improved only when virions came from macrophages. This reflected better cell penetration and correlated with antigenic changes in the virion fusion complex. Macrophages were seen to contact acutely infected epithelial cells, and cre/lox-based virus tagging showed that almost all the virus recovered from lymphoid tissue had passed through lysM(+) and CD11c(+) myeloid cells. Thus MuHV-4 reached B cells in 3 distinct stages: incoming virions infected epithelial cells; infection then passed to myeloid cells; glycoprotein changes then allowed B cell infection. These data identify new complexity in rhadinovirus infection and potentially also new vulnerability to intervention.
format	article
author	Bruno Frederico Ricardo Milho Janet S May Laurent Gillet Philip G Stevenson
author_facet	Bruno Frederico Ricardo Milho Janet S May Laurent Gillet Philip G Stevenson
author_sort	Bruno Frederico
title	Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
title_short	Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
title_full	Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
title_fullStr	Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
title_full_unstemmed	Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.
title_sort	myeloid infection links epithelial and b cell tropisms of murid herpesvirus-4.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/78884973648844a49b0d65b544b96ed1
work_keys_str_mv	AT brunofrederico myeloidinfectionlinksepithelialandbcelltropismsofmuridherpesvirus4 AT ricardomilho myeloidinfectionlinksepithelialandbcelltropismsofmuridherpesvirus4 AT janetsmay myeloidinfectionlinksepithelialandbcelltropismsofmuridherpesvirus4 AT laurentgillet myeloidinfectionlinksepithelialandbcelltropismsofmuridherpesvirus4 AT philipgstevenson myeloidinfectionlinksepithelialandbcelltropismsofmuridherpesvirus4
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Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.

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