The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization

Herpesviruses maintain long-term infectivity without marked antigenic variation. They must therefore evade neutralization by other means. Immune sera block murine gammaherpesvirus-68 (MHV-68) infection of fibroblasts, but fail to block and even enhance its infection of IgG Fc receptor-bearing cells,...

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Main Authors:	Gillet, Laurent, May, Janet S., Colaco, Susanna, Stevenson, Philip G.
Format:	Online
Language:	English
Published:	Public Library of Science 2007
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1931612/

id	pubmed-1931612
recordtype	oai_dc
spelling	pubmed-19316122007-08-08 The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization Gillet, Laurent May, Janet S. Colaco, Susanna Stevenson, Philip G. Research Article Herpesviruses maintain long-term infectivity without marked antigenic variation. They must therefore evade neutralization by other means. Immune sera block murine gammaherpesvirus-68 (MHV-68) infection of fibroblasts, but fail to block and even enhance its infection of IgG Fc receptor-bearing cells, suggesting that the antibody response to infection is actually poor at ablating virion infectivity completely. Here we analyzed this effect further by quantitating the glycoprotein-specific antibody response of MHV-68 carrier mice. Gp150 was much the commonest glycoprotein target and played a predominant role in driving Fc receptor-dependent infection: when gp150-specific antibodies were boosted, Fc receptor-dependent infection increased; and when gp150-specific antibodies were removed, Fc receptor-dependent infection was largely lost. Neither gp150-specific monoclonal antibodies nor gp150-specific polyclonal sera gave significant virion neutralization. Gp150 therefore acts as an immunogenic decoy, distorting the MHV-68-specific antibody response to promote Fc receptor-dependent infection and so compromise virion neutralization. This immune evasion mechanism may be common to many non-essential herpesvirus glycoproteins. Public Library of Science 2007-08-08 /pmc/articles/PMC1931612/ /pubmed/17684552 http://dx.doi.org/10.1371/journal.pone.0000705 Text en Gillet et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Gillet, Laurent May, Janet S. Colaco, Susanna Stevenson, Philip G.
spellingShingle	Gillet, Laurent May, Janet S. Colaco, Susanna Stevenson, Philip G. The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
author_facet	Gillet, Laurent May, Janet S. Colaco, Susanna Stevenson, Philip G.
author_sort	Gillet, Laurent
title	The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
title_short	The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
title_full	The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
title_fullStr	The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
title_full_unstemmed	The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization
title_sort	murine gammaherpesvirus-68 gp150 acts as an immunogenic decoy to limit virion neutralization
description	Herpesviruses maintain long-term infectivity without marked antigenic variation. They must therefore evade neutralization by other means. Immune sera block murine gammaherpesvirus-68 (MHV-68) infection of fibroblasts, but fail to block and even enhance its infection of IgG Fc receptor-bearing cells, suggesting that the antibody response to infection is actually poor at ablating virion infectivity completely. Here we analyzed this effect further by quantitating the glycoprotein-specific antibody response of MHV-68 carrier mice. Gp150 was much the commonest glycoprotein target and played a predominant role in driving Fc receptor-dependent infection: when gp150-specific antibodies were boosted, Fc receptor-dependent infection increased; and when gp150-specific antibodies were removed, Fc receptor-dependent infection was largely lost. Neither gp150-specific monoclonal antibodies nor gp150-specific polyclonal sera gave significant virion neutralization. Gp150 therefore acts as an immunogenic decoy, distorting the MHV-68-specific antibody response to promote Fc receptor-dependent infection and so compromise virion neutralization. This immune evasion mechanism may be common to many non-essential herpesvirus glycoproteins.
publisher	Public Library of Science
publishDate	2007
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1931612/
_version_	1611398538516758528

The Murine Gammaherpesvirus-68 gp150 Acts as an Immunogenic Decoy to Limit Virion Neutralization

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