Imperial College London

Professor Michael A. ("Mike") Skinner

Faculty of MedicineDepartment of Infectious Disease

Emeritus Professor in Virology
 
 
 
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Contact

 

+44 (0)20 7594 3938m.skinner Website

 
 
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Assistant

 

Mrs Yasmin Mallu +44 (0)20 7594 3972

 
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Location

 

315Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

159 results found

Kennedy GM, Murphy SJ, Lisse CM, Menard F, Sitko ML, Wyatt MC, Bayliss DDR, DeMeo FE, Crawford KB, Kim DL, Rudy RJ, Russell RW, Sibthorpe B, Skinner MA, Zhou Get al., 2014, Evolution from protoplanetary to debris discs: the transition disc around HD 166191, MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Vol: 438, Pages: 3299-3309, ISSN: 0035-8711

Journal article

Edgehouse M, Brown TJ, Colon AJ, Cromwell WC, Schwimmer BS, Skinner MA, Walton DMet al., 2013, Diet of a Population of Western Terrestrial Garter Snake, <i>Thamnophis elegans</i>, along the Grande Ronde River, Southeastern Washington, NORTHWEST SCIENCE, Vol: 87, Pages: 349-353, ISSN: 0029-344X

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

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

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

Schat KA, Skinner MA, 2013, Avian Immunosuppressive Diseases and Immunoevasion, Pages: 275-297

Subclinical immunosuppression in chickens is an important but often underestimated factor in the subsequent development of clinical disease. Immunosuppression can be caused by pathogens such as chicken infectious anemia virus, infectious bursal disease virus, reovirus, and some retroviruses (e.g., reticuloendotheliosis virus). Mycotoxins and stress, often caused by poor management practices, can also cause immunosuppression. The effects on the innate and acquired immune responses and the mechanisms by which mycotoxins, stress and infectious agents cause immunosuppression are discussed. Immunoevasion is a common ploy by which viruses neutralize or evade immune responses. DNA viruses such as herpesvirus and poxvirus have multiple genes, some of them host-derived, which interfere with effective innate or acquired immune responses. RNA viruses may escape acquired humoral and cellular immune responses by mutations in protective antigenic epitopes (e.g., avian influenza viruses), while accessory non-structural proteins or multi-functional structural proteins interfere with the interferon system (e.g., Newcastle disease virus). © 2014 Elsevier Ltd All rights reserved.

Journal article

Skinner MA, Laidlaw SM, 2012, Recombinant Avipoxviruses, Vaccinology: Principles and Practice, Editors: Morrow, Schmidt, Sheikh, Davies, Publisher: Wiley-Blackwell

Book chapter

Diesen DL, Skinner MA, 2012, Pediatric thyroid cancer, SEMINARS IN PEDIATRIC SURGERY, Vol: 21, Pages: 44-50, ISSN: 1055-8586

Journal article

Alder AC, Thornton J, McHard K, Buckins L, Barber R, Skinner MAet al., 2011, A comparison of traditional incision and drainage versus catheter drainage of soft tissue abscesses in children, JOURNAL OF PEDIATRIC SURGERY, Vol: 46, Pages: 1942-1947, ISSN: 0022-3468

Journal article

Skinner MA, Buller RM, Damon IK, Lefkowiz EJ, McFadden G, McInnes C J, Mercer AA, Moyer R W, Upton Cet al., 2011, Family: Poxviridae, Virus Taxonomy - Ninth Report of the International Committee on Taxonomy of Viruses, Editors: King, Lefkowitz, Adams, Carstens, Publisher: Elsevier Science Ltd, ISBN: 9780123846846

Book chapter

Bridge SH, Sharpe SA, Dennis MJ, Dowall SD, Getty B, Anson DS, Skinner MA, Stewart JP, Blanchard TJet al., 2011, Heterologous prime-boost-boost immunisation of Chinese cynomolgus macaques using DNA and recombinant poxvirus vectors expressing HIV-1 virus-like particles, VIROLOGY JOURNAL, Vol: 8, ISSN: 1743-422X

Journal article

Trim RD, Skinner MA, Farone MB, DuBois JD, Newsome ALet al., 2011, Use of PCR to detect Entamoeba gingivalis in diseased gingival pockets and demonstrate its absence in healthy gingival sites, PARASITOLOGY RESEARCH, Vol: 109, Pages: 857-864, ISSN: 0932-0113

Journal article

Galindo CL, McIver LJ, Tae H, McCormick JF, Skinner MA, Hoeschele I, Lewis CM, Minna JD, Boothman DA, Garner HRet al., 2011, Sporadic Breast Cancer Patients' Germline DNA Exhibit an AT-Rich Microsatellite Signature, GENES CHROMOSOMES & CANCER, Vol: 50, Pages: 275-283, ISSN: 1045-2257

Journal article

Jeshtadi A, Burgos P, Stubbs CD, Parker AW, King LA, Skinner MA, Botchway SWet al., 2010, Interaction of poxvirus intracellular mature virion proteins with the TPR domain of kinesin light chain in live infected cells revealed by two-photon-induced fluorescence resonance energy transfer fluorescence lifetime imaging microscopy., Journal of Virology, Vol: 84, Pages: 12886-12894, ISSN: 1098-5514

Using two-photon-induced fluorescence lifetime imaging microscopy, we corroborate an interaction (previously demonstrated by yeast two-hybrid domain analysis) of full-length vaccinia virus (VACV; an orthopoxvirus) A36 protein with the cellular microtubule motor protein kinesin. Quenching of enhanced green fluorescent protein (EGFP), fused to the C terminus of VACV A36, by monomeric red fluorescent protein (mDsRed), fused to the tetratricopeptide repeat (TPR) domain of kinesin, was observed in live chicken embryo fibroblasts infected with either modified vaccinia virus Ankara (MVA) or wild-type fowlpox virus (FWPV; an avipoxvirus), and the excited-state fluorescence lifetime of EGFP was reduced from 2.5 ± 0.1 ns to 2.1 ± 0.1 ns due to resonance energy transfer to mDsRed. FWPV does not encode an equivalent of intracellular enveloped virion surface protein A36, yet it is likely that this virus too must interact with kinesin to facilitate intracellular virion transport. To investigate possible interactions between innate FWPV proteins and kinesin, recombinant FWPVs expressing EGFP fused to the N termini of FWPV structural proteins Fpv140, Fpv168, Fpv191, and Fpv198 (equivalent to VACV H3, A4, p4c, and A34, respectively) were generated. EGFP fusions of intracellular mature virion (IMV) surface protein Fpv140 and type II membrane protein Fpv198 were quenched by mDsRed-TPR in recombinant FWPV-infected cells, indicating that these virion proteins are found within 10 nm of mDsRed-TPR. In contrast, and as expected, EGFP fusions of the IMV core protein Fpv168 did not show any quenching. Interestingly, the p4c-like protein Fpv191, which demonstrates late association with preassembled IMV, also did not show any quenching.

Journal article

Chinn IK, Olson JA, Skinner MA, McCarthy EA, Gupton SE, Chen D-F, Bonilla FA, Roberts RL, Kanariou MG, Devlin BH, Markert MLet al., 2010, Mechanisms of tolerance to parental parathyroid tissue when combined with human allogeneic thymus transplantation, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 126, Pages: 814-U208, ISSN: 0091-6749

Journal article

Errami M, Sun Z, George AC, Long TC, Skinner MA, Wren JD, Garner HRet al., 2010, Identifying duplicate content using statistically improbable phrases, BIOINFORMATICS, Vol: 26, Pages: 1453-1457, ISSN: 1367-4803

Journal article

Bridge S, Sharpe S, Dennis M, Dowall S, Getty B, Skinner M, Hahn B, Stewart J, Blanchard Tet al., 2010, HIV-neutralising response to recombinant, cross-clade, adjuvanted, virus-like particle-forming vaccine candidates, HIV MEDICINE, Vol: 11, Pages: 40-40, ISSN: 1464-2662

Journal article

Chinn IK, Olson JA, Skinner MA, McCarthy EA, Gupton SE, Bonilla FA, Roberts RL, Kanariou MG, Devlin BH, Markert MLet al., 2010, Mechanisms of Tolerance to Parental Parathyroid Tissue when Combined with Human Allogeneic Thymus Transplantation, 66th Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology, Publisher: MOSBY-ELSEVIER, Pages: AB55-AB55, ISSN: 0091-6749

Conference paper

Skinner MA, Laidlaw SM, 2009, Advances in fowlpox vaccination, CAB Reviews: Perspectives in Agriculture, Veterinary Science, Nutrition and Natural Resources, Vol: 4, Pages: 1-10

Journal article

Perley DA, Li W, Chornock R, Prochaska JX, Butler NR, Chandra P, Pollack LK, Bloom JS, Filippenko AV, Swan H, Yuan F, Akerlof C, Auger MW, Cenko SB, Chen H-W, Fassnacht CD, Fox D, Frail D, Johansson EM, McKay T, Le Mignant D, Modjaz M, Rujopakarn W, Russel R, Skinner MA, Smith GH, Smith I, van Dam MA, Yost Set al., 2008, GRB 071003: BROADBAND FOLLOW-UP OBSERVATIONS OF A VERY BRIGHT GAMMA-RAY BURST IN A GALACTIC HALO, ASTROPHYSICAL JOURNAL, Vol: 688, Pages: 470-490, ISSN: 0004-637X

Journal article

Skinner MA, Lackey KE, Freemerman AJ, 2008, RET activation inhibits doxorubicin-induced apoptosis in SK-N-MC cells, ANTICANCER RESEARCH, Vol: 28, Pages: 2019-2025, ISSN: 0250-7005

Journal article

Markert ML, Li J, Devlin BH, Hoehner JC, Rice HE, Skinner MA, Li Y-J, Hale LPet al., 2008, Use of allograft biopsies to assess thymopoiesis after thymus transplantation, JOURNAL OF IMMUNOLOGY, Vol: 180, Pages: 6354-6364, ISSN: 0022-1767

Journal article

Skinner MA, 2008, Fowlpox virus and other avipoxviruses, Encyclopedia of Virology, Editors: Mahy, Van Regenmortel, Publisher: Academic Press, ISBN: 9780123739353

Book chapter

Smith GL, Beard P, Skinner MA, 2008, Poxviruses, Encyclopedia of Virology, Editors: Mahy, Van Regenmortel, Publisher: Academic Press, ISBN: 978-0-12-373935-3

Book chapter

Guzman E, Taylor G, Charleston B, Skinner MA, Ellis SAet al., 2008, An MHC-restricted CD8<SUP>+</SUP> T-cell response is induced in cattle by foot-and-mouth disease virus (FMDV) infection and also following vaccination with inactivated FMDV, JOURNAL OF GENERAL VIROLOGY, Vol: 89, Pages: 667-675, ISSN: 0022-1317

Journal article

Chinni IK, Olson JA, Skinner MA, McCarthy EA, Gupton SE, Bonilla FA, Roberts RL, Kanariou MG, Devlin BH, Markert MLet al., 2008, Combined thymus and parathyroid allotransplantation in complete DiGeorge anomaly, 64th Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology, Publisher: MOSBY-ELSEVIER, Pages: S269-S269, ISSN: 0091-6749

Conference paper

Skinner MA, Safford SD, Reeves JG, Jackson ME, Freemerman AJet al., 2008, Renal aplasia in humans is associated with <i>RET</i> mutations, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 82, Pages: 344-351, ISSN: 0002-9297

Journal article

Smith GL, Beard P, Skinner MA, 2008, Poxviruses, Encyclopedia of Virology: Volume 1-5, ISBN: 9780123739353

The family Poxviridae comprises an eclectic group of large, complex viruses that have been isolated from insects, reptiles, birds, marsupials, and mammals. These viruses are distinguished by replication in the cytoplasm, large double-stranded DNA genomes with terminal hairpins, numerous virus-encoded enzymes for transcription and DNA replication, unique modes of morphogenesis and virus entry, and many virulence factors to combat the host response to infection. The most infamous member of this group is variola virus, the cause of smallpox, a disease declared eradicated in 1979. Most poxviruses cause acute diseases of short duration, though some cause lesions that can persist for several months. This article introduces the classification, virion structure, genome structure, gene content, phylogeny, replication cycle, and pathogenesis of poxviruses.

Book chapter

Skinner MA, 2008, Fowlpox Virus and Other Avipoxviruses, Encyclopedia of Virology: Volume 1-5, ISBN: 9780123739353

Poxvirus infections of avian species worldwide are caused by viruses of a single genus ( Avipoxvirus), one of the eight genera of the subfamily Chordopoxvirinae (all of which infect vertebrates) of the family Poxviridae. Viruses of the other seven genera all infect mammals. Even though they can enter mammalian cells and initiate virus gene expression, none of the known avipoxviruses appear capable of causing disease in mammals, despite ample opportunity for such infections to occur. They therefore appear to pose no direct threat to humans or other mammals. In common with other poxviruses, avipoxviruses contain (within complex, multilayered virions) single, covalently closed, linear, double-stranded DNA genomes (the largest known poxviral genomes, with sizes up to more than 300 kbp) and replicate within the cytoplasm of the cells they infect.

Book chapter

Schat KA, Skinner MA, 2008, Avian Immunosuppressive Diseases and Immune Evasion, Avian Immunology, Editors: Davison, Kaspers, Schat, Publisher: Elsevier, Pages: 301-324, ISBN: 9780123706348

Book chapter

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