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The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections
γδ T cells are activated in viral, bacterial and parasitic infections. Among viruses that promote γδ T cell mobilisation in humans, herpes viruses (HHVs) occupy a particular place since they infect the majority of the human population and persist indefinitely in the organism in a latent state. Thus,...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8704314/ https://www.ncbi.nlm.nih.gov/pubmed/34960641 http://dx.doi.org/10.3390/v13122372 |
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author | Martini, Fanny Champagne, Eric |
author_facet | Martini, Fanny Champagne, Eric |
author_sort | Martini, Fanny |
collection | PubMed |
description | γδ T cells are activated in viral, bacterial and parasitic infections. Among viruses that promote γδ T cell mobilisation in humans, herpes viruses (HHVs) occupy a particular place since they infect the majority of the human population and persist indefinitely in the organism in a latent state. Thus, other infections should, in most instances, be considered co-infections, and the reactivation of HHV is a serious confounding factor in attributing γδ T cell alterations to a particular pathogen in human diseases. We review here the literature data on γδ T cell mobilisation in HHV infections and co-infections, and discuss the possible contribution of HHVs to γδ alterations observed in various infectious settings. As multiple infections seemingly mobilise overlapping γδ subsets, we also address the concept of possible cross-protection. |
format | Online Article Text |
id | pubmed-8704314 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-87043142021-12-25 The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections Martini, Fanny Champagne, Eric Viruses Review γδ T cells are activated in viral, bacterial and parasitic infections. Among viruses that promote γδ T cell mobilisation in humans, herpes viruses (HHVs) occupy a particular place since they infect the majority of the human population and persist indefinitely in the organism in a latent state. Thus, other infections should, in most instances, be considered co-infections, and the reactivation of HHV is a serious confounding factor in attributing γδ T cell alterations to a particular pathogen in human diseases. We review here the literature data on γδ T cell mobilisation in HHV infections and co-infections, and discuss the possible contribution of HHVs to γδ alterations observed in various infectious settings. As multiple infections seemingly mobilise overlapping γδ subsets, we also address the concept of possible cross-protection. MDPI 2021-11-26 /pmc/articles/PMC8704314/ /pubmed/34960641 http://dx.doi.org/10.3390/v13122372 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Martini, Fanny Champagne, Eric The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title | The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title_full | The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title_fullStr | The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title_full_unstemmed | The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title_short | The Contribution of Human Herpes Viruses to γδ T Cell Mobilisation in Co-Infections |
title_sort | contribution of human herpes viruses to γδ t cell mobilisation in co-infections |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8704314/ https://www.ncbi.nlm.nih.gov/pubmed/34960641 http://dx.doi.org/10.3390/v13122372 |
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