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).
, , , , ,
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{Peacock:2020:10.1128/JVI.00132-20,
author = {Peacock, TP and Swann, OC and Salvesen, HA and Staller, E and Leung, PB and Goldhill, DH and Zhou, H and Lillico, SG and Whitelaw, CBA and Long, JS and Barclay, WS},
doi = {10.1128/JVI.00132-20},
journal = {Journal of Virology},
title = {Swine ANP32A supports avian influenza virus polymerase.},
url = {http://dx.doi.org/10.1128/JVI.00132-20},
volume = {94},
year = {2020}
}
TY - JOUR
AB - Avian influenza viruses occasionally infect and adapt to mammals, including humans. Swine are often described as 'mixing vessels', being susceptible to both avian and human origin viruses, which allows the emergence of novel reassortants, such as the precursor to the 2009 H1N1 pandemic. ANP32 proteins are host factors that act as influenza virus polymerase cofactors. In this study we describe how swine ANP32A, uniquely among the mammalian ANP32 proteins tested, supports activity of avian origin influenza virus polymerases, and avian influenza virus replication. We further show that after the swine-origin influenza virus emerged in humans and caused the 2009 pandemic it evolved polymerase gene mutations that enabled it to more efficiently use human ANP32 proteins. We map the enhanced pro-viral activity of swine ANP32A to a pair of amino acids, 106 and 156, in the leucine-rich repeat and central domains and show these mutations enhance binding to influenza virus trimeric polymerase. These findings help elucidate the molecular basis for the 'mixing vessel' trait of swine and further our understanding of the evolution and ecology of viruses in this host.Importance Avian influenza viruses can jump from wild birds and poultry into mammalian species such as humans or swine, but only continue to transmit if they accumulate mammalian adapting mutations. Pigs appear uniquely susceptible to both avian and human strains of influenza and are often described as virus 'mixing vessels'. In this study, we describe how a host factor responsible for regulating virus replication, ANP32A, is different between swine and humans. Swine ANP32A allows a greater range of influenza viruses, specifically those from birds, to replicate. It does this through binding the virus polymerase more tightly than the human version of the protein. This work helps to explain the unique properties of swine as 'mixing vessels'.
AU - Peacock,TP
AU - Swann,OC
AU - Salvesen,HA
AU - Staller,E
AU - Leung,PB
AU - Goldhill,DH
AU - Zhou,H
AU - Lillico,SG
AU - Whitelaw,CBA
AU - Long,JS
AU - Barclay,WS
DO - 10.1128/JVI.00132-20
PY - 2020///
SN - 0022-538X
TI - Swine ANP32A supports avian influenza virus polymerase.
T2 - Journal of Virology
UR - http://dx.doi.org/10.1128/JVI.00132-20
UR - https://www.ncbi.nlm.nih.gov/pubmed/32269123
UR - https://jvi.asm.org/content/early/2020/04/02/JVI.00132-20
UR - http://hdl.handle.net/10044/1/78522
VL - 94
ER -