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Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection

Canine influenza virus (CIV) subtype H3N2 is a newly identified, highly contagious respiratory pathogen that causes cough, pneumonia and other respiratory symptoms in dogs. Data indicate that the virus is responsible for recent clinical cases of dog disease in China. However, therapeutic options for...

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Autores principales: Xie, Xing, Lin, Yan, Pang, Maoda, Zhao, Yanbing, Kalhoro, Dildar Hussain, Lu, Chengping, Liu, Yongjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364502/
https://www.ncbi.nlm.nih.gov/pubmed/25888728
http://dx.doi.org/10.1186/s13567-015-0146-7
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author Xie, Xing
Lin, Yan
Pang, Maoda
Zhao, Yanbing
Kalhoro, Dildar Hussain
Lu, Chengping
Liu, Yongjie
author_facet Xie, Xing
Lin, Yan
Pang, Maoda
Zhao, Yanbing
Kalhoro, Dildar Hussain
Lu, Chengping
Liu, Yongjie
author_sort Xie, Xing
collection PubMed
description Canine influenza virus (CIV) subtype H3N2 is a newly identified, highly contagious respiratory pathogen that causes cough, pneumonia and other respiratory symptoms in dogs. Data indicate that the virus is responsible for recent clinical cases of dog disease in China. However, therapeutic options for this disease are very limited. In this study, seven monoclonal antibodies (mAbs) against CIV JS/10 (an H3N2 subtype virus) were produced and characterized. Among them, mAb D7, which is specific for the HA2 glycopeptide (gp), induced the highest neutralization titers. The protection provided by mAb D7 was evaluated in BALB/c mice challenged with homologous or heterologous strains of H3N2 influenza virus, including two strains of CIV and one strain of swine influenza virus (SIV). The data show that mAb D7 protected the mice from infection with the three viral strains, especially the homologous strain, which was indicated by the recovery of body weight, reduction of viral load, and reduction of tissue damage. Moreover, the levels of IFN-γ and TNF-α in the lungs, as detected by ELISA, were reduced in the infected mice treated with the mAb D7 compared with those without mAb D7 treatment. Thus, our findings demonstrate, for the first time, that a mAb could reduce the release of IFN-γ and TNF-α associated with tissue damage by CIV infection and that the mAb might be of great therapeutic value for CIV infection. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-015-0146-7) contains supplementary material, which is available to authorized users.
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spelling pubmed-43645022015-03-19 Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection Xie, Xing Lin, Yan Pang, Maoda Zhao, Yanbing Kalhoro, Dildar Hussain Lu, Chengping Liu, Yongjie Vet Res Research Canine influenza virus (CIV) subtype H3N2 is a newly identified, highly contagious respiratory pathogen that causes cough, pneumonia and other respiratory symptoms in dogs. Data indicate that the virus is responsible for recent clinical cases of dog disease in China. However, therapeutic options for this disease are very limited. In this study, seven monoclonal antibodies (mAbs) against CIV JS/10 (an H3N2 subtype virus) were produced and characterized. Among them, mAb D7, which is specific for the HA2 glycopeptide (gp), induced the highest neutralization titers. The protection provided by mAb D7 was evaluated in BALB/c mice challenged with homologous or heterologous strains of H3N2 influenza virus, including two strains of CIV and one strain of swine influenza virus (SIV). The data show that mAb D7 protected the mice from infection with the three viral strains, especially the homologous strain, which was indicated by the recovery of body weight, reduction of viral load, and reduction of tissue damage. Moreover, the levels of IFN-γ and TNF-α in the lungs, as detected by ELISA, were reduced in the infected mice treated with the mAb D7 compared with those without mAb D7 treatment. Thus, our findings demonstrate, for the first time, that a mAb could reduce the release of IFN-γ and TNF-α associated with tissue damage by CIV infection and that the mAb might be of great therapeutic value for CIV infection. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13567-015-0146-7) contains supplementary material, which is available to authorized users. BioMed Central 2015-03-19 2015 /pmc/articles/PMC4364502/ /pubmed/25888728 http://dx.doi.org/10.1186/s13567-015-0146-7 Text en © Xie et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Xie, Xing
Lin, Yan
Pang, Maoda
Zhao, Yanbing
Kalhoro, Dildar Hussain
Lu, Chengping
Liu, Yongjie
Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title_full Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title_fullStr Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title_full_unstemmed Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title_short Monoclonal antibody specific to HA2 glycopeptide protects mice from H3N2 influenza virus infection
title_sort monoclonal antibody specific to ha2 glycopeptide protects mice from h3n2 influenza virus infection
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364502/
https://www.ncbi.nlm.nih.gov/pubmed/25888728
http://dx.doi.org/10.1186/s13567-015-0146-7
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