In this section
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:2015:10.12688/f1000research.6085.2,
author = {Long, J and Wright, E and Molesti, E and Temperton, N and Barclay, W},
doi = {10.12688/f1000research.6085.2},
journal = {F1000 Research},
pages = {30--30},
title = {Antiviral therapies against Ebola and other emerging viral diseases using existing medicines that block virus entry.},
url = {http://dx.doi.org/10.12688/f1000research.6085.2},
volume = {4},
year = {2015}
}
TY - JOUR
AB - Emerging viral diseases pose a threat to the global population as intervention strategies are mainly limited to basic containment due to the lack of efficacious and approved vaccines and antiviral drugs. The former was the only available intervention when the current unprecedented Ebolavirus (EBOV) outbreak in West Africa began. Prior to this, the development of EBOV vaccines and anti-viral therapies required time and resources that were not available. Therefore, focus has turned to re-purposing of existing, licenced medicines that may limit the morbidity and mortality rates of EBOV and could be used immediately. Here we test three such medicines and measure their ability to inhibit pseudotype viruses (PVs) of two EBOV species, Marburg virus (MARV) and avian influenza H5 (FLU-H5). We confirm the ability of chloroquine (CQ) to inhibit viral entry in a pH specific manner. The commonly used proton pump inhibitors, Omeprazole and Esomeprazole were also able to inhibit entry of all PVs tested but at higher drug concentrations than may be achieved in vivo. We propose CQ as a priority candidate to consider for treatment of EBOV.
AU - Long,J
AU - Wright,E
AU - Molesti,E
AU - Temperton,N
AU - Barclay,W
DO - 10.12688/f1000research.6085.2
EP - 30
PY - 2015///
SN - 2046-1402
SP - 30
TI - Antiviral therapies against Ebola and other emerging viral diseases using existing medicines that block virus entry.
T2 - F1000 Research
UR - http://dx.doi.org/10.12688/f1000research.6085.2
UR - http://hdl.handle.net/10044/1/28770
VL - 4
ER -
For any enquiries related to this group, please contact:
Professor Wendy Barclay
Chair in Influenza Virology
+44 (020) 7594 5035
w.barclay@imperial.ac.uk