Author summary Varicella zoster virus (VZV) causes two main pathologies in humans, chickenpox during primary infection, and shingles following reactivation. The latter is a painful condition that is often followed by chronic pain in a large numbers of shingles patients. Despite the existence of a vaccine, shingles-related complications cause expenses of more than $1 billion per year in the USA alone. Following primary infection, the virus infects leukocytes including T cells, spreading to the skin causing chickenpox. Direct infection of neurons from leukocytes has also been postulated. Given the relevance of leukocytes in VZV biology and the importance of chemokines in directing their migration, we investigated whether VZV modulates the function of chemokines. Our results show that VZV glycoprotein C potentiates the activity of chemokines, inducing higher migration of human leukocytes at low chemokine concentration. This may attract additional susceptible leukocytes to the site of infection enhancing virus spread and pathogenesis.
%0 Journal Article
%1 10.1371/journal.ppat.1006346
%A González-Motos, V
%A Jürgens, C
%A Ritter, B
%A Kropp, K A
%A Durán, V
%A Larsen, O
%A Binz, A
%A Ouwendijk, W J D
%A Lenac Rovis, T
%A Jonjic, S
%A Verjans, G M G M
%A Sodeik, B
%A Krey, T
%A Bauerfeind, R
%A Schulz, T F
%A Kaufer, B B
%A Kalinke, U
%A Proudfoot, A E I
%A Rosenkilde, M M
%A Viejo-Borbolla, A
%D 2017
%E Pathog, PLoS
%I Public Library of Science
%J PLoS Pathog
%K Kalinke
%N 5
%P 1-28
%T Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration
%U https://doi.org/10.1371/journal.ppat.1006346
%V 13
%X Author summary Varicella zoster virus (VZV) causes two main pathologies in humans, chickenpox during primary infection, and shingles following reactivation. The latter is a painful condition that is often followed by chronic pain in a large numbers of shingles patients. Despite the existence of a vaccine, shingles-related complications cause expenses of more than $1 billion per year in the USA alone. Following primary infection, the virus infects leukocytes including T cells, spreading to the skin causing chickenpox. Direct infection of neurons from leukocytes has also been postulated. Given the relevance of leukocytes in VZV biology and the importance of chemokines in directing their migration, we investigated whether VZV modulates the function of chemokines. Our results show that VZV glycoprotein C potentiates the activity of chemokines, inducing higher migration of human leukocytes at low chemokine concentration. This may attract additional susceptible leukocytes to the site of infection enhancing virus spread and pathogenesis.
@article{10.1371/journal.ppat.1006346,
abstract = {Author summary Varicella zoster virus (VZV) causes two main pathologies in humans, chickenpox during primary infection, and shingles following reactivation. The latter is a painful condition that is often followed by chronic pain in a large numbers of shingles patients. Despite the existence of a vaccine, shingles-related complications cause expenses of more than $1 billion per year in the USA alone. Following primary infection, the virus infects leukocytes including T cells, spreading to the skin causing chickenpox. Direct infection of neurons from leukocytes has also been postulated. Given the relevance of leukocytes in VZV biology and the importance of chemokines in directing their migration, we investigated whether VZV modulates the function of chemokines. Our results show that VZV glycoprotein C potentiates the activity of chemokines, inducing higher migration of human leukocytes at low chemokine concentration. This may attract additional susceptible leukocytes to the site of infection enhancing virus spread and pathogenesis.},
added-at = {2017-05-30T12:17:14.000+0200},
author = {González-Motos, V and Jürgens, C and Ritter, B and Kropp, K A and Durán, V and Larsen, O and Binz, A and Ouwendijk, W J D and Lenac Rovis, T and Jonjic, S and Verjans, G M G M and Sodeik, B and Krey, T and Bauerfeind, R and Schulz, T F and Kaufer, B B and Kalinke, U and Proudfoot, A E I and Rosenkilde, M M and Viejo-Borbolla, A},
biburl = {https://www.bibsonomy.org/bibtex/20407899e3a9c2528e8042c43c4aa2f2c/kalinke},
editor = {Pathog, PLoS},
interhash = {d3589700aaa8042aded2a5bf4ddb4b3d},
intrahash = {0407899e3a9c2528e8042c43c4aa2f2c},
journal = {PLoS Pathog},
keywords = {Kalinke},
month = {05},
number = 5,
pages = {1-28},
publisher = {Public Library of Science},
pubmedurl = {https://www.ncbi.nlm.nih.gov/pubmed/28542541},
timestamp = {2017-05-30T12:17:14.000+0200},
title = {Varicella zoster virus glycoprotein C increases chemokine-mediated leukocyte migration},
url = {https://doi.org/10.1371/journal.ppat.1006346},
volume = 13,
year = 2017
}