[Source: PLoS One, full page: (LINK). Abstract, edited.]
Open Access / Peer-reviewed / Research Article
Antibodies to Antigenic Site A of Influenza H7 Hemagglutinin Provide Protection against H7N9 Challenge [ ]
Published: January 28, 2015 / DOI: 10.1371/journal.pone.0117108
Identifying major antigenic and protective epitopes of the H7 hemagglutinin (HA) will be important for understanding the antibody response to vaccines developed against the novel influenza H7N9 viruses that emerged in China in 2013. To facilitate antigenic characterization of the H7N9 HA and to develop reagents for evaluation of H7N9 candidate vaccines, we generated a panel of murine monoclonal antibodies (mAbs) to the HA of A/Shanghai/2/2013 using mammalian cell-derived virus-like particles (VLP) containing the H7 HA. Neutralizing antibodies identified an HA epitope corresponding to antigenic site A on the structurally similar influenza H3 hemagglutinin. Importantly, the neutralizing antibodies protect against A/Shanghai/2/2013 challenge. This antigenic site is conserved among many H7 viruses, including strains of both Eurasian and North American lineage, and the isolated neutralizing antibodies are cross-reactive with older H7 vaccine strains. The results indicate that the identified antigenic site is a potentially important protective epitope and suggest the potential benefit of cross-reactive antibody responses to vaccination with H7 candidate vaccines.
Citation:Schmeisser F, Vasudevan A, Verma S, Wang W, Alvarado E, et al. (2015) Antibodies to Antigenic Site A of Influenza H7 Hemagglutinin Provide Protection against H7N9 Challenge. PLoS ONE 10(1): e0117108. doi:10.1371/journal.pone.0117108
Academic Editor: Florian Krammer, Icahn School of Medicine at Mount Sinai, UNITED STATES
Received: October 10, 2014; Accepted: December 19, 2014; Published: January 28, 2015
This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication
Data Availability:All relevant data are within the paper.
Funding:This work was supported by the U.S. Food and Drug Administration and by the Biomedical Advanced Research and Development Authority, Department of Health and Human Services. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.