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:2016:10.1038/nature16474,
author = {Long, J and Efstathios, SG and Moncorge, O and Frise, R and Mistry, B and James, J and Morrison, M and Iqbal, M and Vignal, A and Skinner, MA and Barclay, WS},
doi = {10.1038/nature16474},
journal = {Nature},
pages = {101--104},
title = {Species difference in ANP32A underlies influenza A virus polymerase host restriction},
url = {http://dx.doi.org/10.1038/nature16474},
volume = {529},
year = {2016}
}
TY - JOUR
AB - Influenza pandemics occur unpredictably when zoonotic influenza viruses with novel antigenicity acquire the ability to transmit amongst humans1. Host range breaches are limited by incompatibilities between avian virus components and the human host. Barriers include receptor preference, virion stability and poor activity of the avian virus RNA-dependent RNA polymerase in human cells2. Mutants of the heterotrimeric viral polymerase components, particularly PB2 protein, are selected during mammalian adaptation, but their mode of action is unknown3, 4, 5, 6. We show that a species-specific difference in host protein ANP32A accounts for the suboptimal function of avian virus polymerase in mammalian cells. Avian ANP32A possesses an additional 33 amino acids between the leucine-rich repeats and carboxy-terminal low-complexity acidic region domains. In mammalian cells, avian ANP32A rescued the suboptimal function of avian virus polymerase to levels similar to mammalian-adapted polymerase. Deletion of the avian-specific sequence from chicken ANP32A abrogated this activity, whereas its insertion into human ANP32A, or closely related ANP32B, supported avian virus polymerase function. Substitutions, such as PB2(E627K), were rapidly selected upon infection of humans with avian H5N1 or H7N9 influenza viruses, adapting the viral polymerase for the shorter mammalian ANP32A. Thus ANP32A represents an essential host partner co-opted to support influenza virus replication and is a candidate host target for novel antivirals.
AU - Long,J
AU - Efstathios,SG
AU - Moncorge,O
AU - Frise,R
AU - Mistry,B
AU - James,J
AU - Morrison,M
AU - Iqbal,M
AU - Vignal,A
AU - Skinner,MA
AU - Barclay,WS
DO - 10.1038/nature16474
EP - 104
PY - 2016///
SN - 1476-4687
SP - 101
TI - Species difference in ANP32A underlies influenza A virus polymerase host restriction
T2 - Nature
UR - http://dx.doi.org/10.1038/nature16474
UR - https://www.nature.com/articles/nature16474
UR - http://hdl.handle.net/10044/1/30302
VL - 529
ER -