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. GoldhillAartjan J. W. te VelthuisRobert A. FletcherPinky LangatMaria ZambonAngie 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{Elderfield:2016:10.1099/jgv.0.000386,
author = {Elderfield, RA and Koutsakos, M and Frise, R and Bradley, K and Ashcroft, JW and Shahjahan, M and Lackenby, A and Barclay, WS},
doi = {10.1099/jgv.0.000386},
journal = {Journal of General Virology},
pages = {593--601},
title = {NB protein does not affect Influenza B virus replication in vitro and is not required for replication in or transmission between ferrets.},
url = {http://dx.doi.org/10.1099/jgv.0.000386},
volume = {97},
year = {2016}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - The influenza B virus encodes a unique protein, NB, a membrane protein whose function in the replication cycle is not, as yet, understood. We engineered a recombinant influenza B virus lacking NB expression with no concomitant difference in expression or activity of viral neuraminidase protein, an important caveat since NA is encoded on the same segment and initiated from a start codon just 4 nucleotides downstream of NB. Replication of the virus lacking NB was not different to wild type virus with full length NB in clonal immortalized or complex primary cell cultures. In the mouse model, virus lacking NB induced slightly lower IFN levels in infected lungs but this did not affect virus titres or weight loss. In ferrets infected with a mixture of viruses that did or did not express NB, there was no fitness advantage for the virus that retained NB. Moreover, virus lacking NB protein was transmitted following respiratory droplet exposure of sentinel animals. These data suggest no role for NB in supporting replication or transmission in vivo in this animal model. The role of NB and the nature of selection to retain it in all natural influenza B viruses remain unclear.
AU - Elderfield,RA
AU - Koutsakos,M
AU - Frise,R
AU - Bradley,K
AU - Ashcroft,JW
AU - Shahjahan,M
AU - Lackenby,A
AU - Barclay,WS
DO - 10.1099/jgv.0.000386
EP - 601
PY - 2016///
SN - 1465-2099
SP - 593
TI - NB protein does not affect Influenza B virus replication in vitro and is not required for replication in or transmission between ferrets.
T2 - Journal of General Virology
UR - http://dx.doi.org/10.1099/jgv.0.000386
UR - http://hdl.handle.net/10044/1/29183
VL - 97
ER -