In this section
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{Long:2019:10.7554/eLife.45066,
author = {Long, JS and Idoko-Akoh, A and Mistry, B and Goldhill, D and Staller, E and Schreyer, J and Ross, C and Goodbourn, S and Shelton, H and Skinner, MA and Sang, H and McGrew, MJ and Barclay, W},
doi = {10.7554/eLife.45066},
journal = {eLife},
pages = {1--22},
title = {Species specific differences in use of ANP32 proteins by influenza A virus},
url = {http://dx.doi.org/10.7554/eLife.45066},
volume = {8},
year = {2019}
}
TY - JOUR
AB - Influenza A viruses (IAV) are subject to species barriers that prevent frequent zoonotic transmission and pandemics. One of these barriers is the poor activity of avian IAV polymerases in human cells. Differences between avian and mammalian ANP32 proteins underlie this host range barrier. Human ANP32A and ANP32B homologues both support function of human-adapted influenza polymerase but do not support efficient activity of avian IAV polymerase which requires avian ANP32A. We show here that the gene currently designated as avian ANP32B is evolutionarily distinct from mammalian ANP32B, and that chicken ANP32B does not support IAV polymerase activity even of human-adapted viruses. Consequently, IAV relies solely on chicken ANP32A to support its replication in chicken cells. Amino acids 129I and 130N, accounted for the inactivity of chicken ANP32B. Transfer of these residues to chicken ANP32A abolished support of IAV polymerase. Understanding ANP32 function will help develop antiviral strategies and aid the design of influenza virus resilient genome edited chickens.
AU - Long,JS
AU - Idoko-Akoh,A
AU - Mistry,B
AU - Goldhill,D
AU - Staller,E
AU - Schreyer,J
AU - Ross,C
AU - Goodbourn,S
AU - Shelton,H
AU - Skinner,MA
AU - Sang,H
AU - McGrew,MJ
AU - Barclay,W
DO - 10.7554/eLife.45066
EP - 22
PY - 2019///
SN - 2050-084X
SP - 1
TI - Species specific differences in use of ANP32 proteins by influenza A virus
T2 - eLife
UR - http://dx.doi.org/10.7554/eLife.45066
UR - https://elifesciences.org/articles/45066
UR - http://hdl.handle.net/10044/1/70347
VL - 8
ER -
For any enquiries related to this group, please contact:
Professor Wendy Barclay
Chair in Influenza Virology
+44 (020) 7594 5035
w.barclay@imperial.ac.uk