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.

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  • Journal article
    Elderfield RA, Watson SJ, Godlee A, Adamson WE, Thompson CI, Dunning J, Fernandez-Alonso M, Blumenkrantz D, Hussell T, MOSAIC Investigators, Zambon M, Openshaw P, Kellam P, Barclay WSet al., 2014,

    Accumulation of human-adapting mutations during circulation of A(H1N1)pdm09 influenza virus in humans in the United Kingdom.

    , Journal of virology, Vol: 88, Pages: 13269-13283, ISSN: 0022-538X

    <h4>Unlabelled</h4>The influenza pandemic that emerged in 2009 provided an unprecedented opportunity to study adaptation of a virus recently acquired from an animal source during human transmission. In the United Kingdom, the novel virus spread in three temporally distinct waves between 2009 and 2011. Phylogenetic analysis of complete viral genomes showed that mutations accumulated over time. Second- and third-wave viruses replicated more rapidly in human airway epithelial (HAE) cells than did the first-wave virus. In infected mice, weight loss varied between viral isolates from the same wave but showed no distinct pattern with wave and did not correlate with viral load in the mouse lungs or severity of disease in the human donor. However, second- and third-wave viruses induced less alpha interferon in the infected mouse lungs. NS1 protein, an interferon antagonist, had accumulated several mutations in second- and third-wave viruses. Recombinant viruses with the third-wave NS gene induced less interferon in human cells, but this alone did not account for increased virus fitness in HAE cells. Mutations in HA and NA genes in third-wave viruses caused increased binding to α-2,6-sialic acid and enhanced infectivity in human mucus. A recombinant virus with these two segments replicated more efficiently in HAE cells. A mutation in PA (N321K) enhanced polymerase activity of third-wave viruses and also provided a replicative advantage in HAE cells. Therefore, multiple mutations allowed incremental changes in viral fitness, which together may have contributed to the apparent increase in severity of A(H1N1)pdm09 influenza virus during successive waves.<h4>Importance</h4>Although most people infected with the 2009 pandemic influenza virus had mild or unapparent symptoms, some suffered severe and devastating disease. The reasons for this variability were unknown, but the numbers of severe cases increased during successive waves of human infection i
  • Journal article
    Jia N, Barclay WS, Roberts K, Yen H-L, Chan RWY, Lam AKY, Air G, Peiris JSM, Dell A, Nicholls JM, Haslam SMet al., 2014,

    Glycomic characterization of respiratory tract tissues of ferrets IMPLICATIONS FOR ITS USE IN INFLUENZA VIRUS INFECTION STUDIES

    , Journal of Biological Chemistry, Vol: 289, Pages: 28489-28504, ISSN: 0021-9258

    The initial recognition between influenza virus and the host cell is mediated by interactions between the viral surface protein hemagglutinin and sialic acid-terminated glycoconjugates on the host cell surface. The sialic acid residues can be linked to the adjacent monosaccharide by α2–3- or α2–6-type glycosidic bonds. It is this linkage difference that primarily defines the species barrier of the influenza virus infection with α2–3 binding being associated with avian influenza viruses and α2–6 binding being associated with human strains. The ferret has been extensively used as an animal model to study the transmission of influenza. To better understand the validity of this model system, we undertook glycomic characterization of respiratory tissues of ferret, which allows a comparison of potential viral receptors to be made between humans and ferrets. To complement the structural analysis, lectin staining experiments were performed to characterize the regional distributions of glycans along the respiratory tract of ferrets. Finally, the binding between the glycans identified and the hemagglutinins of different strains of influenza viruses was assessed by glycan array experiments. Our data indicated that the respiratory tissues of ferret heterogeneously express both α2–3- and α2–6-linked sialic acids. However, the respiratory tissues of ferret also expressed the Sda epitope (NeuAcα2-3(GalNAcβ1–4)Galβ1–4GlcNAc) and sialylated N,N′-diacetyllactosamine (NeuAcα2–6GalNAcβ1–4GlcNAc), which have not been observed in the human respiratory tract surface epithelium. The presence of the Sda epitope reduces potential binding sites for avian viruses and thus may have implications for the usefulness of the ferret in the study of influenza virus infection.
  • Journal article
    Goujon C, Moncorge O, Bauby H, Doyle T, Barclay WS, Malim MHet al., 2014,

    Transfer of the Amino-Terminal Nuclear Envelope Targeting Domain of Human MX2 Converts MX1 into an HIV-1 Resistance Factor

    , JOURNAL OF VIROLOGY, Vol: 88, Pages: 9017-9026, ISSN: 0022-538X
  • Journal article
    Cauldwell AV, Long JS, Moncorge O, Barclay WSet al., 2014,

    Viral determinants of influenza A virus host range

    , JOURNAL OF GENERAL VIROLOGY, Vol: 95, Pages: 1193-1210, ISSN: 0022-1317
  • Journal article
    Marriott AC, Dove BK, Whittaker CJ, Bruce C, Ryan KA, Bean TJ, Rayner E, Pearson G, Taylor I, Dowall S, Plank J, Newman E, Barclay WS, Dimmock NJ, Easton AJ, Hallis B, Silman NJ, Carroll MWet al., 2014,

    Low Dose Influenza Virus Challenge in the Ferret Leads to Increased Virus Shedding and Greater Sensitivity to Oseltamivir

    , PLOS ONE, Vol: 9, ISSN: 1932-6203
  • Journal article
    Macdonald DC, Singh H, Whelan MA, Escors D, Arce F, Bottoms SE, Barclay WS, Maini M, Collins MK, Rosenberg WMCet al., 2014,

    Harnessing alveolar macrophages for sustained mucosal T-cell recall confers long-term protection to mice against lethal influenza challenge without clinical disease

    , MUCOSAL IMMUNOLOGY, Vol: 7, Pages: 89-100, ISSN: 1933-0219
  • Journal article
    Goujon C, Moncorge O, Bauby H, Doyle T, Ward CC, Schaller T, Hue S, Barclay WS, Schulz R, Malim MHet al., 2013,

    Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection

    , NATURE, Vol: 502, Pages: 559-+, ISSN: 0028-0836
  • Journal article
    Blumenkrantz D, Roberts KL, Shelton H, Lycett S, Barclay WSet al., 2013,

    The Short Stalk Length of Highly Pathogenic Avian Influenza H5N1 Virus Neuraminidase Limits Transmission of Pandemic H1N1 Virus in Ferrets

    , JOURNAL OF VIROLOGY, Vol: 87, Pages: 10539-10551, ISSN: 0022-538X
  • Journal article
    Sridhar S, Begom S, Bermingham A, Hoschler K, Adamson W, Carman W, Bean T, Barclay W, Deeks JJ, Lalvani Aet al., 2013,

    Cellular immune correlates of protection against symptomatic pandemic influenza

    , Nature Medicine, Vol: n/a, ISSN: 1078-8956
  • Journal article
    Long JS, Howard WA, Nunez A, Moncorge O, Lycett S, Banks J, Barclay WSet al., 2013,

    The Effect of the PB2 Mutation 627K on Highly Pathogenic H5N1 Avian Influenza Virus Is Dependent on the Virus Lineage

    , JOURNAL OF VIROLOGY, Vol: 87, Pages: 9983-9996, ISSN: 0022-538X

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Contact us

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