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{Dunning:2018:10.1038/s41590-018-0111-5,
author = {Dunning, J and Blankley, S and Hoang, LT and Cox, M and Graham, CM and James, PL and Bloom, CI and Chaussabel, D and Banchereau, J and Brett, SJ and Moffatt, MF and OGarra, A and Openshaw, PJM},
doi = {10.1038/s41590-018-0111-5},
journal = {Nature Immunology},
pages = {625--635},
title = {Progression of whole-blood transcriptional signatures from interferon-induced to neutrophil-associated patterns in severe influenza},
url = {http://dx.doi.org/10.1038/s41590-018-0111-5},
volume = {19},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Transcriptional profiles and host-response biomarkers are used increasingly to investigate the severity, subtype and pathogenesis of disease. We now describe whole-blood mRNA signatures and concentrations of local and systemic immunological mediators in 131 adults hospitalized with influenza, from whom extensive clinical and investigational data were obtained by MOSAIC investigators. Signatures reflective of interferon-related antiviral pathways were common up to day 4 of symptoms in patients who did not require mechanical ventilator support; in those who needed mechanical ventilation, an inflammatory, activated-neutrophil and cell-stress or death (‘bacterial’) pattern was seen, even early in disease. Identifiable bacterial co-infection was not necessary for this ‘bacterial’ signature but was able to enhance its development while attenuating the early ‘viral’ signature. Our findings emphasize the importance of timing and severity in the interpretation of host responses to acute viral infection and identify specific patterns of immune-system activation that might enable the development of novel diagnostic and therapeutic tools for severe influenza.
AU - Dunning,J
AU - Blankley,S
AU - Hoang,LT
AU - Cox,M
AU - Graham,CM
AU - James,PL
AU - Bloom,CI
AU - Chaussabel,D
AU - Banchereau,J
AU - Brett,SJ
AU - Moffatt,MF
AU - OGarra,A
AU - Openshaw,PJM
DO - 10.1038/s41590-018-0111-5
EP - 635
PY - 2018///
SN - 1529-2916
SP - 625
TI - Progression of whole-blood transcriptional signatures from interferon-induced to neutrophil-associated patterns in severe influenza
T2 - Nature Immunology
UR - http://dx.doi.org/10.1038/s41590-018-0111-5
UR - https://doi.org/10.1038/s41590-018-0111-5
UR - https://www.nature.com/articles/s41590-018-0111-5
UR - http://hdl.handle.net/10044/1/60073
VL - 19
ER -