Loading…

Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions

1 Division of Virology, Department of Pathology, University of Cambridge, UK 2 Immunobiology Ltd, Babraham Research Campus, Cambridge, UK Correspondence Philip G. Stevenson pgs27{at}cam.ac.uk Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpe...

Full description

Saved in:
Bibliographic Details
Published in:Journal of general virology 2009-11, Vol.90 (11), p.2592-2603
Main Authors: Wright, Debbie E, Colaco, Susanna, Colaco, Camilo, Stevenson, Philip G
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513
cites cdi_FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513
container_end_page 2603
container_issue 11
container_start_page 2592
container_title Journal of general virology
container_volume 90
creator Wright, Debbie E
Colaco, Susanna
Colaco, Camilo
Stevenson, Philip G
description 1 Division of Virology, Department of Pathology, University of Cambridge, UK 2 Immunobiology Ltd, Babraham Research Campus, Cambridge, UK Correspondence Philip G. Stevenson pgs27{at}cam.ac.uk Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization.
doi_str_mv 10.1099/vir.0.014266-0
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2885036</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67685293</sourcerecordid><originalsourceid>FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513</originalsourceid><addsrcrecordid>eNpVkc2L1DAYxoMo7rh69Si5KHjomI8mTS7CsrgfsOBFr4Y0fTsTaZOatLPMf2_KDOt6CuT9vc_zJA9C7ynZUqL1l4NPW7IltGZSVuQF2tBaioqV0Uu0IYSxinLaXKA3Of8mBatF8xpdUC2ZqIXeoF9XYfZt7I548KOfM_YBH_wh4nFJvsN7SBPkYrLkqsYJpsE7O_sYcHvE97tbfOPKrYNpjqnqYILQQZhxvwS3UvktetXbIcO783mJft58-3F9Vz18v72_vnqoXC3YXPWWK-sIW-M1kjvROWic7J1UnWZU1lp1oLhiVLSqIQQU40CI60WjOQjKL9HXk-60tCOU7TAnO5gp-dGmo4nWm_8nwe_NLh4MU0oQLovAp7NAin8WyLMZfXYwDDZAXLKRjVSCaV7A7Ql0KeacoH8yocSslZjyW4aYUyWGlIUPz6P9w88dFODjGbDZ2aFPNjifnzjGiNS1Wt_4-cTt_W7_6BOYHYTRlxytj6urLgGoYUIz_hf7X6SQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67685293</pqid></control><display><type>article</type><title>Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions</title><source>Freely Accessible Science Journals - check A-Z of ejournals</source><creator>Wright, Debbie E ; Colaco, Susanna ; Colaco, Camilo ; Stevenson, Philip G</creator><creatorcontrib>Wright, Debbie E ; Colaco, Susanna ; Colaco, Camilo ; Stevenson, Philip G</creatorcontrib><description>1 Division of Virology, Department of Pathology, University of Cambridge, UK 2 Immunobiology Ltd, Babraham Research Campus, Cambridge, UK Correspondence Philip G. Stevenson pgs27{at}cam.ac.uk Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization.</description><identifier>ISSN: 0022-1317</identifier><identifier>EISSN: 1465-2099</identifier><identifier>DOI: 10.1099/vir.0.014266-0</identifier><identifier>PMID: 19625459</identifier><identifier>CODEN: JGVIAY</identifier><language>eng</language><publisher>Reading: Soc General Microbiol</publisher><subject>Adoptive Transfer ; Animal ; Animals ; Antibodies, Monoclonal - immunology ; Antibodies, Viral - immunology ; Biological and medical sciences ; Fundamental and applied biological sciences. Psychology ; Immunoglobulin G - immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Microbiology ; Miscellaneous ; Neutralization Tests ; Receptors, Fc - immunology ; Rhadinovirus - immunology ; Rhadinovirus - physiology ; Serum - virology ; Viral Plaque Assay ; Virology ; Virus Replication ; Whole Body Imaging</subject><ispartof>Journal of general virology, 2009-11, Vol.90 (11), p.2592-2603</ispartof><rights>2009 INIST-CNRS</rights><rights>Copyright © 2009, SGM 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513</citedby><cites>FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=22069481$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19625459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wright, Debbie E</creatorcontrib><creatorcontrib>Colaco, Susanna</creatorcontrib><creatorcontrib>Colaco, Camilo</creatorcontrib><creatorcontrib>Stevenson, Philip G</creatorcontrib><title>Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions</title><title>Journal of general virology</title><addtitle>J Gen Virol</addtitle><description>1 Division of Virology, Department of Pathology, University of Cambridge, UK 2 Immunobiology Ltd, Babraham Research Campus, Cambridge, UK Correspondence Philip G. Stevenson pgs27{at}cam.ac.uk Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization.</description><subject>Adoptive Transfer</subject><subject>Animal</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antibodies, Viral - immunology</subject><subject>Biological and medical sciences</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunoglobulin G - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Neutralization Tests</subject><subject>Receptors, Fc - immunology</subject><subject>Rhadinovirus - immunology</subject><subject>Rhadinovirus - physiology</subject><subject>Serum - virology</subject><subject>Viral Plaque Assay</subject><subject>Virology</subject><subject>Virus Replication</subject><subject>Whole Body Imaging</subject><issn>0022-1317</issn><issn>1465-2099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNpVkc2L1DAYxoMo7rh69Si5KHjomI8mTS7CsrgfsOBFr4Y0fTsTaZOatLPMf2_KDOt6CuT9vc_zJA9C7ynZUqL1l4NPW7IltGZSVuQF2tBaioqV0Uu0IYSxinLaXKA3Of8mBatF8xpdUC2ZqIXeoF9XYfZt7I548KOfM_YBH_wh4nFJvsN7SBPkYrLkqsYJpsE7O_sYcHvE97tbfOPKrYNpjqnqYILQQZhxvwS3UvktetXbIcO783mJft58-3F9Vz18v72_vnqoXC3YXPWWK-sIW-M1kjvROWic7J1UnWZU1lp1oLhiVLSqIQQU40CI60WjOQjKL9HXk-60tCOU7TAnO5gp-dGmo4nWm_8nwe_NLh4MU0oQLovAp7NAin8WyLMZfXYwDDZAXLKRjVSCaV7A7Ql0KeacoH8yocSslZjyW4aYUyWGlIUPz6P9w88dFODjGbDZ2aFPNjifnzjGiNS1Wt_4-cTt_W7_6BOYHYTRlxytj6urLgGoYUIz_hf7X6SQ</recordid><startdate>20091101</startdate><enddate>20091101</enddate><creator>Wright, Debbie E</creator><creator>Colaco, Susanna</creator><creator>Colaco, Camilo</creator><creator>Stevenson, Philip G</creator><general>Soc General Microbiol</general><general>Society for General Microbiology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20091101</creationdate><title>Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions</title><author>Wright, Debbie E ; Colaco, Susanna ; Colaco, Camilo ; Stevenson, Philip G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adoptive Transfer</topic><topic>Animal</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antibodies, Viral - immunology</topic><topic>Biological and medical sciences</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunoglobulin G - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Neutralization Tests</topic><topic>Receptors, Fc - immunology</topic><topic>Rhadinovirus - immunology</topic><topic>Rhadinovirus - physiology</topic><topic>Serum - virology</topic><topic>Viral Plaque Assay</topic><topic>Virology</topic><topic>Virus Replication</topic><topic>Whole Body Imaging</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wright, Debbie E</creatorcontrib><creatorcontrib>Colaco, Susanna</creatorcontrib><creatorcontrib>Colaco, Camilo</creatorcontrib><creatorcontrib>Stevenson, Philip G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of general virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wright, Debbie E</au><au>Colaco, Susanna</au><au>Colaco, Camilo</au><au>Stevenson, Philip G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions</atitle><jtitle>Journal of general virology</jtitle><addtitle>J Gen Virol</addtitle><date>2009-11-01</date><risdate>2009</risdate><volume>90</volume><issue>11</issue><spage>2592</spage><epage>2603</epage><pages>2592-2603</pages><issn>0022-1317</issn><eissn>1465-2099</eissn><coden>JGVIAY</coden><abstract>1 Division of Virology, Department of Pathology, University of Cambridge, UK 2 Immunobiology Ltd, Babraham Research Campus, Cambridge, UK Correspondence Philip G. Stevenson pgs27{at}cam.ac.uk Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization.</abstract><cop>Reading</cop><pub>Soc General Microbiol</pub><pmid>19625459</pmid><doi>10.1099/vir.0.014266-0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0022-1317
ispartof Journal of general virology, 2009-11, Vol.90 (11), p.2592-2603
issn 0022-1317
1465-2099
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2885036
source Freely Accessible Science Journals - check A-Z of ejournals
subjects Adoptive Transfer
Animal
Animals
Antibodies, Monoclonal - immunology
Antibodies, Viral - immunology
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Immunoglobulin G - immunology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Microbiology
Miscellaneous
Neutralization Tests
Receptors, Fc - immunology
Rhadinovirus - immunology
Rhadinovirus - physiology
Serum - virology
Viral Plaque Assay
Virology
Virus Replication
Whole Body Imaging
title Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T06%3A33%3A59IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antibody%20limits%20in%20vivo%20murid%20herpesvirus-4%20replication%20by%20IgG%20Fc%20receptor-dependent%20functions&rft.jtitle=Journal%20of%20general%20virology&rft.au=Wright,%20Debbie%20E&rft.date=2009-11-01&rft.volume=90&rft.issue=11&rft.spage=2592&rft.epage=2603&rft.pages=2592-2603&rft.issn=0022-1317&rft.eissn=1465-2099&rft.coden=JGVIAY&rft_id=info:doi/10.1099/vir.0.014266-0&rft_dat=%3Cproquest_pubme%3E67685293%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c452t-fa38ac024457763c5dce7c6fc68d9216498de838215b8700e823e00cf5793e513%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=67685293&rft_id=info:pmid/19625459&rfr_iscdi=true