Notable Recent Publications

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).
Daniel H. Goldhill, Aartjan J. W. te Velthuis, Robert A. Fletcher, Pinky Langat, Maria Zambon, Angie Lackenby & Wendy S. Barclay

This paper showed how influenza could evolve resistance to favipiravir, an antiviral that may be used to treat influenza. The residue that mutated to give resistance was highly conserved suggesting that the mechanism of resistance may be applicable to other RNA viruses.

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.

Citation

BibTex format

@article{Giotis:2019:10.1038/s41564-019-0517-3,
author = {Giotis, ES and Carnell, G and Young, EF and Ghanny, S and Soteropoulos, P and Wang, L-F and Barclay, WS and Skinner, MA and Temperton, N},
doi = {10.1038/s41564-019-0517-3},
journal = {Nature Microbiology},
pages = {2035--2038},
title = {Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor.},
url = {http://dx.doi.org/10.1038/s41564-019-0517-3},
volume = {4},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Haemagglutinin and neuraminidase surface glycoproteins of the bat influenza H17N10 virus neither bind to nor cleave sialic acid receptors, indicating that this virus employs cell entry mechanisms distinct from those of classical influenza A viruses. We observed that certain human haematopoietic cancer cell lines and canine MDCK II cells are susceptible to H17-pseudotyped viruses. We identified the human HLA-DR receptor as an entry mediator for H17 pseudotypes, suggesting that H17N10 possesses zoonotic potential.
AU  - Giotis,ES
AU  - Carnell,G
AU  - Young,EF
AU  - Ghanny,S
AU  - Soteropoulos,P
AU  - Wang,L-F
AU  - Barclay,WS
AU  - Skinner,MA
AU  - Temperton,N
DO  - 10.1038/s41564-019-0517-3
EP  - 2038
PY  - 2019///
SN  - 2058-5276
SP  - 2035
TI  - Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor.
T2  - Nature Microbiology
UR  - http://dx.doi.org/10.1038/s41564-019-0517-3
UR  - https://www.ncbi.nlm.nih.gov/pubmed/31358984
UR  - https://www.nature.com/articles/s41564-019-0517-3
UR  - http://hdl.handle.net/10044/1/73077
VL  - 4
ER  -
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Contact us

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