Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.

Oral herpes is a highly prevalent infection caused by herpes simplex virus 1 (HSV-1). After an initial infection of the oral cavity, HSV-1 remains latent in sensory neurons of the trigeminal ganglia. Episodic reactivation of the virus leads to the formation of mucocutaneous lesions (cold sores), but...

Full description

Bibliographic Details
Main Authors: Yi Zuo, J Charles Whitbeck, Gabriel J Haila, Abraham A Hakim, Paul W Rothlauf, Roselyn J Eisenberg, Gary H Cohen, Claude Krummenacher
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0223299
_version_ 1819012845104267264
author Yi Zuo
J Charles Whitbeck
Gabriel J Haila
Abraham A Hakim
Paul W Rothlauf
Roselyn J Eisenberg
Gary H Cohen
Claude Krummenacher
author_facet Yi Zuo
J Charles Whitbeck
Gabriel J Haila
Abraham A Hakim
Paul W Rothlauf
Roselyn J Eisenberg
Gary H Cohen
Claude Krummenacher
author_sort Yi Zuo
collection DOAJ
description Oral herpes is a highly prevalent infection caused by herpes simplex virus 1 (HSV-1). After an initial infection of the oral cavity, HSV-1 remains latent in sensory neurons of the trigeminal ganglia. Episodic reactivation of the virus leads to the formation of mucocutaneous lesions (cold sores), but asymptomatic reactivation accompanied by viral shedding is more frequent and allows virus spread to new hosts. HSV-1 DNA has been detected in many oral tissues. In particular, HSV-1 can be found in periodontal lesions and several studies associated its presence with more severe periodontitis pathologies. Since gingival fibroblasts may become exposed to salivary components in periodontitis lesions, we analyzed the effect of saliva on HSV-1 and -2 infection of these cells. We observed that human gingival fibroblasts can be infected by HSV-1. However, pre-treatment of these cells with saliva extracts from some but not all individuals led to an increased susceptibility to infection. Furthermore, the active saliva could expand HSV-1 tropism to cells that are normally resistant to infection due to the absence of HSV entry receptors. The active factor in saliva was partially purified and comprised high molecular weight complexes of glycoproteins that included secretory Immunoglobulin A. Interestingly, we observed a broad variation in the activity of saliva between donors suggesting that this activity is selectively present in the population. The active saliva factor, has not been isolated, but may lead to the identification of a relevant biomarker for susceptibility to oral herpes. The presence of a salivary factor that enhances HSV-1 infection may influence the risk of oral herpes and/or the severity of associated oral pathologies.
first_indexed 2024-12-21T01:50:31Z
format Article
id doaj.art-19b45f6d1c2c4508a3b21aa8a313aa93
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-12-21T01:50:31Z
publishDate 2019-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-19b45f6d1c2c4508a3b21aa8a313aa932022-12-21T19:19:54ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-011410e022329910.1371/journal.pone.0223299Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.Yi ZuoJ Charles WhitbeckGabriel J HailaAbraham A HakimPaul W RothlaufRoselyn J EisenbergGary H CohenClaude KrummenacherOral herpes is a highly prevalent infection caused by herpes simplex virus 1 (HSV-1). After an initial infection of the oral cavity, HSV-1 remains latent in sensory neurons of the trigeminal ganglia. Episodic reactivation of the virus leads to the formation of mucocutaneous lesions (cold sores), but asymptomatic reactivation accompanied by viral shedding is more frequent and allows virus spread to new hosts. HSV-1 DNA has been detected in many oral tissues. In particular, HSV-1 can be found in periodontal lesions and several studies associated its presence with more severe periodontitis pathologies. Since gingival fibroblasts may become exposed to salivary components in periodontitis lesions, we analyzed the effect of saliva on HSV-1 and -2 infection of these cells. We observed that human gingival fibroblasts can be infected by HSV-1. However, pre-treatment of these cells with saliva extracts from some but not all individuals led to an increased susceptibility to infection. Furthermore, the active saliva could expand HSV-1 tropism to cells that are normally resistant to infection due to the absence of HSV entry receptors. The active factor in saliva was partially purified and comprised high molecular weight complexes of glycoproteins that included secretory Immunoglobulin A. Interestingly, we observed a broad variation in the activity of saliva between donors suggesting that this activity is selectively present in the population. The active saliva factor, has not been isolated, but may lead to the identification of a relevant biomarker for susceptibility to oral herpes. The presence of a salivary factor that enhances HSV-1 infection may influence the risk of oral herpes and/or the severity of associated oral pathologies.https://doi.org/10.1371/journal.pone.0223299
spellingShingle Yi Zuo
J Charles Whitbeck
Gabriel J Haila
Abraham A Hakim
Paul W Rothlauf
Roselyn J Eisenberg
Gary H Cohen
Claude Krummenacher
Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
PLoS ONE
title Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
title_full Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
title_fullStr Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
title_full_unstemmed Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
title_short Saliva enhances infection of gingival fibroblasts by herpes simplex virus 1.
title_sort saliva enhances infection of gingival fibroblasts by herpes simplex virus 1
url https://doi.org/10.1371/journal.pone.0223299
work_keys_str_mv AT yizuo salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT jcharleswhitbeck salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT gabrieljhaila salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT abrahamahakim salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT paulwrothlauf salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT roselynjeisenberg salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT garyhcohen salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1
AT claudekrummenacher salivaenhancesinfectionofgingivalfibroblastsbyherpessimplexvirus1