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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...
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Published in: | Journal of general virology 2009-11, Vol.90 (11), p.2592-2603 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. |
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ISSN: | 0022-1317 1465-2099 |
DOI: | 10.1099/vir.0.014266-0 |