Murid herpesvirus-4 exploits dendritic cells to infect B cells.

Dendritic cells (DCs) play a central role in initiating immune responses. Some persistent viruses infect DCs and can disrupt their functions in vitro. However, these viruses remain strongly immunogenic in vivo. Thus what role DC infection plays in the pathogenesis of persistent infections is unclear...

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Main Authors: Miguel Gaspar, Janet S May, Soumi Sukla, Bruno Frederico, Michael B Gill, Christopher M Smith, Gabrielle T Belz, Philip G Stevenson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-11-01
Series:PLoS Pathogens
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22102809/pdf/?tool=EBI
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spelling doaj-830c8ca746b345b0b9ab1eb3ea1629392021-04-21T17:30:02ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742011-11-01711e100234610.1371/journal.ppat.1002346Murid herpesvirus-4 exploits dendritic cells to infect B cells.Miguel GasparJanet S MaySoumi SuklaBruno FredericoMichael B GillChristopher M SmithGabrielle T BelzPhilip G StevensonDendritic cells (DCs) play a central role in initiating immune responses. Some persistent viruses infect DCs and can disrupt their functions in vitro. However, these viruses remain strongly immunogenic in vivo. Thus what role DC infection plays in the pathogenesis of persistent infections is unclear. Here we show that a persistent, B cell-tropic gamma-herpesvirus, Murid Herpesvirus-4 (MuHV-4), infects DCs early after host entry, before it establishes a substantial infection of B cells. DC-specific virus marking by cre-lox recombination revealed that a significant fraction of the virus latent in B cells had passed through a DC, and a virus attenuated for replication in DCs was impaired in B cell colonization. In vitro MuHV-4 dramatically altered the DC cytoskeleton, suggesting that it manipulates DC migration and shape in order to spread. MuHV-4 therefore uses DCs to colonize B cells.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22102809/pdf/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Miguel Gaspar
Janet S May
Soumi Sukla
Bruno Frederico
Michael B Gill
Christopher M Smith
Gabrielle T Belz
Philip G Stevenson
spellingShingle Miguel Gaspar
Janet S May
Soumi Sukla
Bruno Frederico
Michael B Gill
Christopher M Smith
Gabrielle T Belz
Philip G Stevenson
Murid herpesvirus-4 exploits dendritic cells to infect B cells.
PLoS Pathogens
author_facet Miguel Gaspar
Janet S May
Soumi Sukla
Bruno Frederico
Michael B Gill
Christopher M Smith
Gabrielle T Belz
Philip G Stevenson
author_sort Miguel Gaspar
title Murid herpesvirus-4 exploits dendritic cells to infect B cells.
title_short Murid herpesvirus-4 exploits dendritic cells to infect B cells.
title_full Murid herpesvirus-4 exploits dendritic cells to infect B cells.
title_fullStr Murid herpesvirus-4 exploits dendritic cells to infect B cells.
title_full_unstemmed Murid herpesvirus-4 exploits dendritic cells to infect B cells.
title_sort murid herpesvirus-4 exploits dendritic cells to infect b cells.
publisher Public Library of Science (PLoS)
series PLoS Pathogens
issn 1553-7366
1553-7374
publishDate 2011-11-01
description Dendritic cells (DCs) play a central role in initiating immune responses. Some persistent viruses infect DCs and can disrupt their functions in vitro. However, these viruses remain strongly immunogenic in vivo. Thus what role DC infection plays in the pathogenesis of persistent infections is unclear. Here we show that a persistent, B cell-tropic gamma-herpesvirus, Murid Herpesvirus-4 (MuHV-4), infects DCs early after host entry, before it establishes a substantial infection of B cells. DC-specific virus marking by cre-lox recombination revealed that a significant fraction of the virus latent in B cells had passed through a DC, and a virus attenuated for replication in DCs was impaired in B cell colonization. In vitro MuHV-4 dramatically altered the DC cytoskeleton, suggesting that it manipulates DC migration and shape in order to spread. MuHV-4 therefore uses DCs to colonize B cells.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22102809/pdf/?tool=EBI
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