Publications

Search or filter publications

Filter by type:

Filter by publication type

Filter by year:

to

Results

  • Showing results for:
  • Reset all filters

Search results

  • Journal article
    Almond MH, Edwards MR, Barclay WS, Johnston SLet al., 2013,

    Obesity and susceptibility to severe outcomes following respiratory viral infection

    , THORAX, Vol: 68, Pages: 684-686, ISSN: 0040-6376
  • Journal article
    Shelton H, Roberts KL, Molesti E, Temperton N, Barclay WSet al., 2013,

    Mutations in haemagglutinin that affect receptor binding and pH stability increase replication of a PR8 influenza virus with H5 HA in the upper respiratory tract of ferrets and may contribute to transmissibility

    , JOURNAL OF GENERAL VIROLOGY, Vol: 94, Pages: 1220-1229, ISSN: 0022-1317
  • Journal article
    Barbosa S, Fasanella G, Carreira S, Llarena M, Fox R, Barreca C, Andrew D, O'Hare Pet al., 2013,

    An Orchestrated Program Regulating Secretory Pathway Genes and Cargos by the Transmembrane Transcription Factor CREB-H

    , TRAFFIC, Vol: 14, Pages: 382-398, ISSN: 1398-9219
  • Journal article
    Laidlaw SM, Robey R, Davies M, Giotis E, Ross C, Buttigieg K, Goodbourn S, Skinner MAet al., 2013,

    Genetic Screen of a Mutant Poxvirus Library Identifies an Ankyrin Repeat Protein Involved in Blocking Induction of Avian Type I Interferon

    , Journal of Virology, Vol: 87, ISSN: 1098-5514

    Mammalian poxviruses, including vaccinia virus (VACV), have evolved multiple mechanisms to evade the host type I interferon (IFN) responses at different levels, with viral proteins targeting IFN induction, signaling and antiviral effector functions. Avian poxviruses (avipoxviruses), which have been developed as recombinant vaccine vectors for permissive (i.e. poultry) and non-permissive (i.e. mammals, including humans) species, encode no obvious equivalents of any of these proteins. We show that fowlpox virus (FWPV) fails to induce chicken IFN-beta (ChIFN2) and is able to block its induction by transfected poly(I:C), an analog of cytoplasmic double-strand (ds) RNA. A broad-scale loss-of-function genetic screen was used to find FWPV-encoded modulators of poly(I:C)-mediated ChIFN2 induction. It identified fpv012, a member of a family of poxvirus genes, highly expanded in the avipoxviruses (31 in FWPV; 51 in canarypox virus (CNPV), representing 15% of the total gene complement), encoding proteins containing N-terminal ankyrin repeats (ANKs) and C-terminal F-box-like motifs. Under ectopic expression, the first ANK of fpv012 is dispensable for inhibitory activity and the CNPV ortholog is also able to inhibit induction of ChIFN2. FWPV defective in fpv012 replicate well in culture and barely induce ChIFN2 during infection, suggesting other factors are involved in blocking IFN induction and resisting the antiviral effectors. Nevertheless, unlike parental and revertant viruses, the mutants induce moderate levels of expression of interferon stimulated genes (ISG), suggesting either that there is sufficient ChIFN2 expression to partially induce the ISGs or the involvement of alternative, IFN-independent pathways, that are also normally blocked by fpv012.
  • Journal article
    Buttigieg K, Laidlaw SM, Ross C, Davies M, Goodbourn S, Skinner MAet al., 2013,

    Genetic Screen of a Library of Chimeric Poxviruses Identifies an Ankyrin Repeat Protein Involved in Resistance to the Avian Type I Interferon Response

    , Journal of Virology, Vol: 87, ISSN: 1098-5514

    Viruses must be able to resist host innate responses, especially the type I interferon (IFN) response. They do so by preventing induction or activity of IFN and/or by resisting the antiviral effectors it induces. Poxviruses are no exception, with many mechanisms identified whereby mammalian poxviruses, notably vaccinia (VACV) but also cowpox and myxoma viruses, are able to evade host IFN responses. Similar mechanisms have not been described for avian poxviruses (avipoxviruses). Restricted for permissive replication to avian hosts, they have received less attention; moreover the avian host responses are less well characterised. We show that the prototypic avipoxvirus, fowlpox virus (FWPV) is highly resistant to the antiviral effects of avian IFN. A gain-of-function genetic screen identified fpv014 as contributing to increased resistance to exogenous recombinant chicken IFN-alpha (ChIFN1). Fpv014 is a member of the large family of poxvirus (especially avipoxvirus) genes that encode proteins containing N-terminal ankyrin repeats (ANKs) and C-terminal F-box-like motifs. By binding the Skp1/Cullin-1 complex, the F-box in such proteins appears to target ligands bound by the ANKs for ubiquitination. Mass spectrometry and immunoblotting demonstrated that tandem affinity-purified, tagged fpv014 was complexed with chicken cullin-1 and Skp-1. Prior infection with an fpv014 knockout mutant of FWPV still blocked transfected poly(I:C)-mediated induction of the IFNbeta (ChIFN2) promoter as effectively as parental FWPV, but the mutant was more sensitive to exogenous ChIFN1. Therefore, unlike the related protein fpv012, fpv014 does not contribute to the FWPV block to induction of ChIFN2, but does confer resistance to an established antiviral state.
  • Journal article
    Gyuranecz M, Foster JT, Dan A, Ip HS, Egstad KF, Parker PG, Higashiguchi JM, Skinner MA, Hofle U, Kreizinger Z, Dorrestein GM, Solt S, Sos E, Kim YJ, Uhart M, Pereda A, Gonzalez-Hein G, Hidalgo H, Blanco JM, Erdelyi Ket al., 2013,

    Worldwide Phylogenetic Relationship of Avian Poxviruses

    , Journal of Virology, Vol: 87, ISSN: 1098-5514

    Poxvirus infections have been found in 230 species of wild and domestic birds worldwide in both terrestrial and marine environments. This ubiquity raises the question of how infection has been transmitted and globally dispersed. We present a comprehensive global phylogeny of 111 novel poxvirus isolates in addition to all available sequences from GenBank. Phylogenetic analysis of Avipoxvirus genus has traditionally relied on one gene region (4b core protein). In this study we have expanded the analyses to include a second locus (DNA polymerase gene), allowing for a more robust phylogenetic framework, finer genetic resolution within specific groups and the detection of potential recombination. Our phylogenetic results reveal several major features of avipoxvirus evolution and ecology and propose an updated avipoxvirus taxonomy, including three novel subclades. The characterization of poxviruses from 57 species of birds in this study extends the current knowledge of their host range and provides the first evidence of the phylogenetic effect of genetic recombination of avipoxviruses. The repeated occurrence of avian family or order-specific grouping within certain clades (e.g. starling poxvirus, falcon poxvirus, raptor poxvirus, etc.) indicates a marked role of host adaptation, while the sharing of poxvirus species within prey-predator systems emphasizes the capacity for cross-species infection and limited host adaptation. Our study provides a broad and comprehensive phylogenetic analysis of the Avipoxvirus genus, an ecologically and environmentally important viral group, to formulate a genome sequencing strategy that will clarify avipoxvirus taxonomy.
  • Journal article
    Brady G, Karstegl CE, Farrell PJ, 2013,

    Novel function of the unique N-terminal region of RUNX1c in B cell growth regulation

    , NUCLEIC ACIDS RESEARCH, Vol: 41, Pages: 1555-1568, ISSN: 0305-1048
  • Journal article
    Fouchier RAM, Garcia-Sastre A, Kawaoka Y, Barclay WS, Bouvier NM, Brown IH, Capua I, Chen H, Compans RW, Couch RB, Cox NJ, Doherty PC, Donis RO, Feldmann H, Guan Y, Katz JM, Kiselev OI, Klenk HD, Kobinger G, Liu J, Liu X, Lowen A, Mettenleiter TC, Osterhaus ADME, Palese P, Peiris JSM, Perez DR, Richt JA, Schultz-Cherry S, Steel J, Subbarao K, Swayne DE, Takimoto T, Tashiro M, Taubenberger JK, Thomas PG, Tripp RA, Tumpey TM, Webby RJ, Webster RGet al., 2013,

    Transmission Studies Resume For Avian Flu

    , SCIENCE, Vol: 339, Pages: 520-521, ISSN: 0036-8075
  • Journal article
    Skalska L, White RE, Parker GA, Turro E, Sinclair AJ, Paschos K, Allday MJet al., 2013,

    Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.

    , PLoS Pathog, Vol: 9

    To explore the role of p16(INK4a) as an intrinsic barrier to B cell transformation by EBV, we transformed primary B cells from an individual homozygous for a deletion in the CDKN2A locus encoding p16(INK4a) and p14(ARF). Using recombinant EBV-BAC viruses expressing conditional EBNA3C (3CHT), we developed a system that allows inactivation of EBNA3C in lymphoblastoid cell lines (LCLs) lacking active p16(INK4a) protein but expressing a functional 14(ARF)-fusion protein (p14/p16). The INK4a locus is epigenetically repressed by EBNA3C--in cooperation with EBNA3A--despite the absence of functional p16(INK4a). Although inactivation of EBNA3C in LCLs from normal B cells leads to an increase in p16(INK4a) and growth arrest, EBNA3C inactivation in the p16(INK4a)-null LCLs has no impact on the rate of proliferation, establishing that the repression of INK4a is a major function of EBNA3C in EBV-driven LCL proliferation. This conditional LCL system allowed us to use microarray analysis to identify and confirm genes regulated specifically by EBNA3C, independently of proliferation changes modulated by the p16(INK4a)-Rb-E2F axis. Infections of normal primary B cells with recombinant EBV-BAC virus from which EBNA3C is deleted or with 3CHT EBV in the absence of activating ligand 4-hydroxytamoxifen, revealed that EBNA3C is necessary to overcome an EBV-driven increase in p16(INK4a) expression and concomitant block to proliferation 2-4 weeks post-infection. If cells are p16(INK4a)-null, functional EBNA3C is dispensable for the outgrowth of LCLs.
  • Journal article
    Cauldwell 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

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

Request URL: http://wwwtest.imperial.ac.uk:80/respub/WEB-INF/jsp/search-t4-html.jsp Request URI: /respub/WEB-INF/jsp/search-t4-html.jsp Query String: id=810&limit=10&page=8&respub-action=search.html Current Millis: 1759578890453 Current Time: Sat Oct 04 12:54:50 BST 2025