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).
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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.
Results
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Journal articleFouchier RAM, Garcia-Sastre A, Kawaoka Y, et al., 2013,
Transmission Studies Resume For Avian Flu
, SCIENCE, Vol: 339, Pages: 520-521, ISSN: 0036-8075- Author Web Link
- Cite
- Citations: 26
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Journal articleCauldwell AV, Moncorge O, Barclay WS, 2013,
Unstable Polymerase-Nucleoprotein Interaction Is Not Responsible for Avian Influenza Virus Polymerase Restriction in Human Cells
, JOURNAL OF VIROLOGY, Vol: 87, Pages: 1278-1284, ISSN: 0022-538X- Author Web Link
- Cite
- Citations: 35
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Journal articleMoncorge O, Long JS, Cauldwell AV, et al., 2013,
Investigation of Influenza Virus Polymerase Activity in Pig Cells
, JOURNAL OF VIROLOGY, Vol: 87, Pages: 384-394, ISSN: 0022-538X- Author Web Link
- Cite
- Citations: 38
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Journal articleIto K, Ashcroft J, Brookes D, et al., 2013,
Inhibitory Effects Of Rv1088, A Narrow Spectrum Kinase Inhibitor, On Cytokine Production In Response To Pandemic Flu Infections Of Primary Respiratory Cell Cultures
, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X -
Journal articleSridhar S, Begom S, Bermingham A, et al., 2012,
Predominance of heterosubtypic IFN-?-only-secreting effector memory T cells in pandemic H1N1 naive adults
, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 42, Pages: 2913-2924, ISSN: 0014-2980- Author Web Link
- Cite
- Citations: 28
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Journal articleRoberts KL, Shelton H, Stilwell P, et al., 2012,
Transmission of a 2009 H1N1 Pandemic Influenza Virus Occurs before Fever Is Detected, in the Ferret Model
, PLOS ONE, Vol: 7, ISSN: 1932-6203- Author Web Link
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- Citations: 32
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Journal articleShelton H, Smith M, Hartgroves L, et al., 2012,
An influenza reassortant with polymerase of pH1N1 and NS gene of H3N2 influenza A virus is attenuated <i>in vivo</i>
, JOURNAL OF GENERAL VIROLOGY, Vol: 93, Pages: 998-1006, ISSN: 0022-1317- Author Web Link
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- Citations: 16
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Journal articleEveritt AR, Clare S, Pertel T, et al., 2012,
IFITM3 restricts the morbidity and mortality associated with influenza.
, Nature, Vol: 484, Pages: 519-523The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses1, 2, 3, 4, 5, 6, 7. Both the magnitude and breadth of the IFITM proteins’ in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model8, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 ‘Spanish’ influenza9, 10. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.
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Journal articleLefevre EA, Carr BV, Inman CF, et al., 2012,
Immune Responses in Pigs Vaccinated with Adjuvanted and Non-Adjuvanted A(H1N1)pdm/09 Influenza Vaccines Used in Human Immunization Programmes
, PLOS One, Vol: 7, ISSN: 1932-6203Following the emergence and global spread of a novel H1N1 influenza virus in 2009, two A(H1N1)pdm/09 influenza vaccines produced from the A/California/07/09 H1N1 strain were selected and used for the national immunisation programme in the United Kingdom: an adjuvanted split virion vaccine and a non-adjuvanted whole virion vaccine. In this study, we assessed the immune responses generated in inbred large white pigs (Babraham line) following vaccination with these vaccines and after challenge with A(H1N1)pdm/09 virus three months post-vaccination. Both vaccines elicited strong antibody responses, which included high levels of influenza-specific IgG1 and haemagglutination inhibition titres to H1 virus. Immunisation with the adjuvanted split vaccine induced significantly higher interferon gamma production, increased frequency of interferon gamma-producing cells and proliferation of CD4−CD8+ (cytotoxic) and CD4+CD8+ (helper) T cells, after in vitro re-stimulation. Despite significant differences in the magnitude and breadth of immune responses in the two vaccinated and mock treated groups, similar quantities of viral RNA were detected from the nasal cavity in all pigs after live virus challenge. The present study provides support for the use of the pig as a valid experimental model for influenza infections in humans, including the assessment of protective efficacy of therapeutic interventions.
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Journal articleFouchier RAM, Garcia-Sastre A, Kawaoka Y, et al., 2012,
Pause on Avian Flu Transmission Research
, SCIENCE, Vol: 335, Pages: 400-401, ISSN: 0036-8075- Author Web Link
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- Citations: 48
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