Publications

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{Rehwinkel:2010:10.1016/j.cell.2010.01.020,
author = {Rehwinkel, J and Tan, CP and Goubau, D and Schulz, O and Pichlmair, A and Bier, K and Robb, N and Vreede, F and Barclay, W and Fodor, E and Reis, e Sousa C},
doi = {10.1016/j.cell.2010.01.020},
journal = {Cell},
pages = {397--408},
title = {RIG-I detects viral genomic RNA during negative-strand RNA virus infection.},
url = {http://dx.doi.org/10.1016/j.cell.2010.01.020},
volume = {140},
year = {2010}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - RIG-I is a key mediator of antiviral immunity, able to couple detection of infection by RNA viruses to the induction of interferons. Natural RIG-I stimulatory RNAs have variously been proposed to correspond to virus genomes, virus replication intermediates, viral transcripts, or self-RNA cleaved by RNase L. However, the relative contribution of each of these RNA species to RIG-I activation and interferon induction in virus-infected cells is not known. Here, we use three approaches to identify physiological RIG-I agonists in cells infected with influenza A virus or Sendai virus. We show that RIG-I agonists are exclusively generated by the process of virus replication and correspond to full-length virus genomes. Therefore, nongenomic viral transcripts, short replication intermediates, and cleaved self-RNA do not contribute substantially to interferon induction in cells infected with these negative strand RNA viruses. Rather, single-stranded RNA viral genomes bearing 5'-triphosphates constitute the natural RIG-I agonists that trigger cell-intrinsic innate immune responses during infection.
AU  - Rehwinkel,J
AU  - Tan,CP
AU  - Goubau,D
AU  - Schulz,O
AU  - Pichlmair,A
AU  - Bier,K
AU  - Robb,N
AU  - Vreede,F
AU  - Barclay,W
AU  - Fodor,E
AU  - Reis,e Sousa C
DO  - 10.1016/j.cell.2010.01.020
EP  - 408
PY  - 2010///
SP  - 397
TI  - RIG-I detects viral genomic RNA during negative-strand RNA virus infection.
T2  - Cell
UR  - http://dx.doi.org/10.1016/j.cell.2010.01.020
VL  - 140
ER  -
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