These are some recent publications which give a flavour of the research from the Barclay lab. For a complete list of publications, please see below.
Species difference in ANP32A underlies influenza A virus polymerase host restriction. Nature (2016).
Jason S. Long, Efstathios S. Giotis, Olivier Moncorgé, Rebecca Frise, Bhakti Mistry, Joe James, Mireille Morisson, Munir Iqbal, Alain Vignal, Michael A. Skinner & Wendy S. Barclay
This paper identified a key factor that explained why the polymerases from avian influenza viruses are restricted in humans. For more, please see the associated New and Views.
See our latest ANP32 papers here: eLIFE, Journal of Virology, Journal of Virology.
The mechanism of resistance to favipiravir in influenza. PNAS (2018).
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Internal genes of a highly pathogenic H5N1 influenza virus determine high viral replication in myeloid cells and severe outcome of infection in mice. Plos Path. (2018).
Hui Li*, Konrad C. Bradley*, Jason S. Long, Rebecca Frise, Jonathan W. Ashcroft, Lorian C. Hartgroves, Holly Shelton, Spyridon Makris, Cecilia Johansson, Bin Cao & Wendy S. Barclay
Why do avian influenza viruses like H5N1 cause such severe disease in humans? This paper demonstrated that H5N1 viruses replicate better than human viruses in myeloid cells from mice leading to a cytokine storm and more severe disease.
@article{Peacock:2016:10.1038/srep18745,
author = {Peacock, T and Reddy, K and James, J and Adamiak, B and Barclay, W and Shelton, H and Iqbal, M},
doi = {10.1038/srep18745},
journal = {Scientific Reports},
title = {Antigenic mapping of an H9N2 avian influenza virus reveals two discrete antigenic sites and a novel mechanism of immune escape},
url = {http://dx.doi.org/10.1038/srep18745},
volume = {6},
year = {2016}
}
TY - JOUR
AB - H9N2 avian influenza virus is a major cause of poultry production loss across Asia leading to the wide useof vaccines. Efficacy of vaccines is often compromised due to the rapid emergence of antigenic variants.To improve the effectiveness of vaccines in the field, a better understanding of the antigenic epitopesof the major antigen, hemagglutinin, is required. To address this, a panel of nine monoclonal antibodieswere generated against a contemporary Pakistani H9N2 isolate, which represents a major Asian H9N2viral lineage. Antibodies were characterized in detail and used to select a total of 26 unique ‘escape’mutants with substitutions across nine different amino acid residues in hemagglutinin including seventhat have not been described as antigenic determinants for H9N2 viruses before. Competition assaysand structural mapping revealed two novel, discrete antigenic sites “H9-A” and “H9-B”. Additionally,a second subset of escape mutants contained amino acid deletions within the hemagglutinin receptorbinding site. This constitutes a novel method of escape for group 1 hemagglutinins and could representan alternative means for H9N2 viruses to overcome vaccine induced immunity. These results will guidesurveillance efforts for arising antigenic variants as well as evidence based vaccine seed selection andvaccine design.
AU - Peacock,T
AU - Reddy,K
AU - James,J
AU - Adamiak,B
AU - Barclay,W
AU - Shelton,H
AU - Iqbal,M
DO - 10.1038/srep18745
PY - 2016///
SN - 2045-2322
TI - Antigenic mapping of an H9N2 avian influenza virus reveals two discrete antigenic sites and a novel mechanism of immune escape
T2 - Scientific Reports
UR - http://dx.doi.org/10.1038/srep18745
UR - http://hdl.handle.net/10044/1/30024
VL - 6
ER -