2.50
Hdl Handle:
http://hdl.handle.net/10033/620941
Title:
Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.
Authors:
González-Motos, Víctor; Jürgens, Carina; Ritter, Birgit; Kropp, Kai A; Durán, Verónica; Larsen, Olav; Binz, Anne; Ouwendijk, Werner J D; Lenac Rovis, Tihana; Jonjic, Stipan; Verjans, Georges M G M; Sodeik, Beate; Krey, Thomas; Bauerfeind, Rudolf; Schulz, Thomas F; Kaufer, Benedikt B; Kalinke, Ulrich ( 0000-0003-0503-9564 ) ; Proudfoot, Amanda E I; Rosenkilde, Mette M; Viejo-Borbolla, Abel
Abstract:
Varicella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans.
Affiliation:
TWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH, Feodor-Lynen Str. 7, 30625 Hannover, Germany.
Citation:
Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration. 2017, 13 (5):e1006346 PLoS Pathog.
Journal:
PLoS pathogens
Issue Date:
May-2017
URI:
http://hdl.handle.net/10033/620941
DOI:
10.1371/journal.ppat.1006346
PubMed ID:
28542541
Type:
Article
Language:
en
ISSN:
1553-7374
Appears in Collections:
publications of the department of experimental infection research ([TC] EXPI)

Full metadata record

DC FieldValue Language
dc.contributor.authorGonzález-Motos, Víctoren
dc.contributor.authorJürgens, Carinaen
dc.contributor.authorRitter, Birgiten
dc.contributor.authorKropp, Kai Aen
dc.contributor.authorDurán, Verónicaen
dc.contributor.authorLarsen, Olaven
dc.contributor.authorBinz, Anneen
dc.contributor.authorOuwendijk, Werner J Den
dc.contributor.authorLenac Rovis, Tihanaen
dc.contributor.authorJonjic, Stipanen
dc.contributor.authorVerjans, Georges M G Men
dc.contributor.authorSodeik, Beateen
dc.contributor.authorKrey, Thomasen
dc.contributor.authorBauerfeind, Rudolfen
dc.contributor.authorSchulz, Thomas Fen
dc.contributor.authorKaufer, Benedikt Ben
dc.contributor.authorKalinke, Ulrichen
dc.contributor.authorProudfoot, Amanda E Ien
dc.contributor.authorRosenkilde, Mette Men
dc.contributor.authorViejo-Borbolla, Abelen
dc.date.accessioned2017-06-12T12:27:43Z-
dc.date.available2017-06-12T12:27:43Z-
dc.date.issued2017-05-
dc.identifier.citationVaricella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration. 2017, 13 (5):e1006346 PLoS Pathog.en
dc.identifier.issn1553-7374-
dc.identifier.pmid28542541-
dc.identifier.doi10.1371/journal.ppat.1006346-
dc.identifier.urihttp://hdl.handle.net/10033/620941-
dc.description.abstractVaricella zoster virus (VZV) is a highly prevalent human pathogen that establishes latency in neurons of the peripheral nervous system. Primary infection causes varicella whereas reactivation results in zoster, which is often followed by chronic pain in adults. Following infection of epithelial cells in the respiratory tract, VZV spreads within the host by hijacking leukocytes, including T cells, in the tonsils and other regional lymph nodes, and modifying their activity. In spite of its importance in pathogenesis, the mechanism of dissemination remains poorly understood. Here we addressed the influence of VZV on leukocyte migration and found that the purified recombinant soluble ectodomain of VZV glycoprotein C (rSgC) binds chemokines with high affinity. Functional experiments show that VZV rSgC potentiates chemokine activity, enhancing the migration of monocyte and T cell lines and, most importantly, human tonsillar leukocytes at low chemokine concentrations. Binding and potentiation of chemokine activity occurs through the C-terminal part of gC ectodomain, containing predicted immunoglobulin-like domains. The mechanism of action of VZV rSgC requires interaction with the chemokine and signalling through the chemokine receptor. Finally, we show that VZV viral particles enhance chemokine-dependent T cell migration and that gC is partially required for this activity. We propose that VZV gC activity facilitates the recruitment and subsequent infection of leukocytes and thereby enhances VZV systemic dissemination in humans.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleVaricella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH, Feodor-Lynen Str. 7, 30625 Hannover, Germany.en
dc.identifier.journalPLoS pathogensen
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