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Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6

Freshly isolated monocytes rapidly undergo physiological changes in vitro, resulting in programmed cell death (apoptosis). Activation of monocytes, which promotes differentiation into macrophages, is known to inhibit apoptotic processes. In the present study, we report that human herpesvirus-6 (HHV-...

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Autores principales: Janelle, M.-E., Flamand, L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087170/
https://www.ncbi.nlm.nih.gov/pubmed/16474928
http://dx.doi.org/10.1007/s00705-005-0715-6
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author Janelle, M.-E.
Flamand, L.
author_facet Janelle, M.-E.
Flamand, L.
author_sort Janelle, M.-E.
collection PubMed
description Freshly isolated monocytes rapidly undergo physiological changes in vitro, resulting in programmed cell death (apoptosis). Activation of monocytes, which promotes differentiation into macrophages, is known to inhibit apoptotic processes. In the present study, we report that human herpesvirus-6 (HHV-6) prevents monocytes from undergoing spontaneous apoptosis during the first 72 hours of culture. Furthermore, significant alterations in cell-surface phenotype were observed after 72 hours of infection with HHV-6. HHV-6-infected monocyte cultures have considerably reduced levels of CD14, CD64 (FcγRI) and HLA-DR antigen on their surface, while CD32 (FcγRII) expression is unaffected. On the basis of these results, we hypothesize that HHV-6 promotes monocytes survival and causes phenotypic modifications that could favor immune evasion and ensure its persistence within the infected host.
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spelling pubmed-70871702020-03-23 Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6 Janelle, M.-E. Flamand, L. Arch Virol Article Freshly isolated monocytes rapidly undergo physiological changes in vitro, resulting in programmed cell death (apoptosis). Activation of monocytes, which promotes differentiation into macrophages, is known to inhibit apoptotic processes. In the present study, we report that human herpesvirus-6 (HHV-6) prevents monocytes from undergoing spontaneous apoptosis during the first 72 hours of culture. Furthermore, significant alterations in cell-surface phenotype were observed after 72 hours of infection with HHV-6. HHV-6-infected monocyte cultures have considerably reduced levels of CD14, CD64 (FcγRI) and HLA-DR antigen on their surface, while CD32 (FcγRII) expression is unaffected. On the basis of these results, we hypothesize that HHV-6 promotes monocytes survival and causes phenotypic modifications that could favor immune evasion and ensure its persistence within the infected host. Springer-Verlag 2006-02-13 2006 /pmc/articles/PMC7087170/ /pubmed/16474928 http://dx.doi.org/10.1007/s00705-005-0715-6 Text en © Springer-Verlag 2006 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
Janelle, M.-E.
Flamand, L.
Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title_full Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title_fullStr Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title_full_unstemmed Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title_short Phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
title_sort phenotypic alterations and survival of monocytes following infection by human herpesvirus-6
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7087170/
https://www.ncbi.nlm.nih.gov/pubmed/16474928
http://dx.doi.org/10.1007/s00705-005-0715-6
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