Imperial College London

Dr Michael A. ("Mike") Skinner

Faculty of MedicineDepartment of Infectious Disease

Reader in Virology
 
 
 
//

Contact

 

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

 
 
//

Assistant

 

Mrs Yasmin Mallu +44 (0)20 7594 3972

 
//

Location

 

315Medical SchoolSt Mary's Campus

//

Summary

 

Publications

Publication Type
Year
to

93 results found

Giotis ES, Carnell G, Young EF, Ghanny S, Soteropoulos P, Wang L-F, Barclay WS, Skinner MA, Temperton Net al., 2019, Entry of the bat influenza H17N10 virus into mammalian cells is enabled by the MHC class II HLA-DR receptor., Nature Microbiology, ISSN: 2058-5276

Haemagglutinin and neuraminidase surface glycoproteins of the bat influenza H17N10 virus neither bind to nor cleave sialic acid receptors, indicating that this virus employs cell entry mechanisms distinct from those of classical influenza A viruses. We observed that certain human haematopoietic cancer cell lines and canine MDCK II cells are susceptible to H17-pseudotyped viruses. We identified the human HLA-DR receptor as an entry mediator for H17 pseudotypes, suggesting that H17N10 possesses zoonotic potential.

Journal article

Long JS, Idoko-Akoh A, Mistry B, Goldhill D, Staller E, Schreyer J, Ross C, Goodbourn S, Shelton H, Skinner MA, Sang H, McGrew MJ, Barclay Wet al., 2019, Species specific differences in use of ANP32 proteins by influenza A virus, eLife, Vol: 8, ISSN: 2050-084X

Influenza A viruses (IAV) are subject to species barriers that prevent frequent zoonotic transmission and pandemics. One of these barriers is the poor activity of avian IAV polymerases in human cells. Differences between avian and mammalian ANP32 proteins underlie this host range barrier. Human ANP32A and ANP32B homologues both support function of human-adapted influenza polymerase but do not support efficient activity of avian IAV polymerase which requires avian ANP32A. We show here that the gene currently designated as avian ANP32B is evolutionarily distinct from mammalian ANP32B, and that chicken ANP32B does not support IAV polymerase activity even of human-adapted viruses. Consequently, IAV relies solely on chicken ANP32A to support its replication in chicken cells. Amino acids 129I and 130N, accounted for the inactivity of chicken ANP32B. Transfer of these residues to chicken ANP32A abolished support of IAV polymerase. Understanding ANP32 function will help develop antiviral strategies and aid the design of influenza virus resilient genome edited chickens.

Journal article

Giotis E, Montillet G, Pain B, Skinner Met al., 2019, Chicken embryonic-stem cells are permissive to poxvirus recombinant vaccine vectors, Genes, Vol: 10, ISSN: 2073-4425

The discovery of mammalian pluripotent embryonic stem cells (ESC) has revolutionised cell research and regenerative medicine. More recently discovered chicken ESC (cESC), though less intensively studied, are increasingly popular as vaccine substrates due to a dearth of avian cell lines. Information on the comparative performance of cESC with common vaccine viruses is limited. Using RNA-sequencing, we compared cESC transcriptional programmes elicited by stimulation with chicken type I interferon or infection with vaccine viruses routinely propagated in primary chicken embryo fibroblasts (CEF). We used poxviruses (fowlpox virus (FWPV) FP9, canarypox virus (CNPV), and modified vaccinia virus Ankara (MVA)) and a birnavirus (infectious bursal disease virus (IBDV) PBG98). Interferon-stimulated genes (ISGs) were induced in cESC to levels comparable to those in CEF and immortalised chicken fibroblast DF-1 cells. cESC are permissive (with distinct host transcriptional responses) to MVA, FP9, and CNPV but, surprisingly, not to PBG98. MVA, CNPV, and FP9 suppressed innate immune responses, while PBG98 induced a subset of ISGs. Dysregulation of signalling pathways (i.e., NFκB, TRAF) was observed, which might affect immune responses and viral replication. In conclusion, we show that cESC are an attractive alternative substrate to study and propagate poxvirus recombinant vaccine vectors.

Journal article

Giotis ES, Skinner M, 2019, Spotlight on avian pathology: fowlpox virus, Avian Pathology, Vol: 48, Pages: 87-90, ISSN: 0307-9457

Fowlpox virus is the type species of an extensive and poorly-defined group of viruses isolated from more than 200 species of birds, together comprising the avipoxvirus genus of the poxvirus family. Long known as a significant poultry pathogen, vaccines developed in the early and middle years of the 20th century led to its effective eradication as a problem to commercial production in temperate climes in developed western countries (such that vaccination there is now far less common). Transmitted mechanically by biting insects, it remains problematic, causing significant losses to all forms of production (from back-yard, through extensive to intensive commercial flocks), in tropical climes where control of biting insects is difficult. In these regions, vaccination (via intra-dermal or subcutaneous, and increasingly in ovo, routes) remains necessary. Although there is no evidence that more than a single serotype exists, there are poorly-described reports of outbreaks in vaccinated flocks. Whether this is due to inadequate vaccination or penetrance of novel variants remains unclear. Some such outbreaks have been associated with strains carrying endogenous, infectious proviral copies of the retrovirus, reticulo-endotheliosis virus (REV), which might represent a pathotypic (if not newly emerging) variant in the field. Until more is known about the phylogenetic structure of the avipoxvirus genus (by more widespread genome sequencing of isolates from different species of birds) it remains difficult to ascertain the risk of novel avipoxviruses emerging from wild birds (and/or by recombination/mutation) to infect farmed poultry.

Journal article

Giotis ES, Ross CS, Robey RC, Nohturfft A, Goodbourn S, Skinner MAet al., 2017, Constitutively elevated levels of SOCS1 suppress innate responses in DF-1 immortalised chicken fibroblast cells, Scientific Reports, Vol: 7, ISSN: 2045-2322

The spontaneously immortalised DF-1 cell line is rapidly replacing its progenitor primary chicken embryo fibroblasts (CEFs) for studies on avian viruses such as avian influenza but no comprehensive study has as yet been reported comparing their innate immunity phenotypes. We conducted microarray analyses of DF-1 and CEFs, under both normal and stimulated conditions using chicken interferon-α (chIFNα) and the attenuated infectious bursal disease virus vaccine strain PBG98. We found that DF-1 have an attenuated innate response compared to CEFs. Basal expression levels of Suppressor of Cytokine Signalling 1 (chSOCS1), a negative regulator of cytokine signalling in mammals, are 16-fold higher in DF-1 than in CEFs. The chSOCS1 “SOCS box” domain (which, in mammals, interacts with an E3 ubiquitin ligase complex) is not essential for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1. Overexpression of SOCS1 in chIFNα-stimulated DF-1 led to a relative decrease in expression of interferon-stimulated genes (ISGs; MX1 and IFIT5) and increased viral yield in response to PBG98 infection. Conversely, knockdown of SOCS1 enhanced induction of ISGs and reduced viral yield in chIFNα-stimulated DF-1. Consequently, SOCS1 reduces induction of the IFN signalling pathway in chicken cells and can potentiate virus replication.

Journal article

Dulwich KL, Giotis ES, Gray A, Nair V, Skinner MA, Broadbent AJet al., 2017, Differential gene expression in chicken primary B cells infected ex vivo with attenuated and very virulent strains of infectious bursal disease virus (IBDV)., Journal of General Virology, Vol: 98, Pages: 2918-2930, ISSN: 1465-2099

Infectious bursal disease virus (IBDV) belongs to the family Birnaviridae and is economically important to the poultry industry worldwide. IBDV infects B cells in the bursa of Fabricius (BF), causing immunosuppression and morbidity in young chickens. In addition to strains that cause classical Gumboro disease, the so-called 'very virulent' (vv) strain, also in circulation, causes more severe disease and increased mortality. IBDV has traditionally been controlled through the use of live attenuated vaccines, with attenuation resulting from serial passage in non-lymphoid cells. However, the factors that contribute to the vv or attenuated phenotypes are poorly understood. In order to address this, we aimed to investigate host cell-IBDV interactions using a recently described chicken primary B-cell model, where chicken B cells are harvested from the BF and cultured ex vivo in the presence of chicken CD40L. We demonstrated that these cells could support the replication of IBDV when infected ex vivo in the laboratory. Furthermore, we evaluated the gene expression profiles of B cells infected with an attenuated strain (D78) and a very virulent strain (UK661) by microarray. We found that key genes involved in B-cell activation and signalling (TNFSF13B, CD72 and GRAP) were down-regulated following infection relative to mock, which we speculate could contribute to IBDV-mediated immunosuppression. Moreover, cells responded to infection by expressing antiviral type I IFNs and IFN-stimulated genes, but the induction was far less pronounced upon infection with UK661, which we speculate could contribute to its virulence.

Journal article

Anasir MI, Caria S, Skinner MA, Kvansakul Met al., 2017, Structural basis of apoptosis inhibition by the Fowlpox virus protein FPV039, Journal of Biological Chemistry, Vol: 292, Pages: 9010-9021, ISSN: 1083-351X

Programmed cell death or apoptosis of infected host cells is an important defense mechanism in response to viral infections. This process is regulated by pro-apoptotic and pro-survival members of the B-cell lymphoma 2 (Bcl-2) protein family. To counter premature death of a virus-infected cell, poxviruses use a range of different molecular strategies, including the mimicry of pro-survival Bcl-2 proteins. One such viral pro-survival protein is the fowlpox virus protein FPV039, which is a potent apoptosis inhibitor, but the precise molecular mechanism by which FPV039 inhibits apoptosis is unknown. To understand how fowlpox virus inhibits apoptosis we examined FPV039 using isothermal titration calorimetry, small-angle X-ray scattering and X-ray crystallography. Here, we report that the fowlpox virus pro-survival protein FPV039 promiscuously binds to cellular pro-apoptotic Bcl-2, and engages all major pro-apoptotic Bcl-2 proteins. Unlike other identified viral Bcl-2 proteins to date, FPV039 engaged with cellular pro-apoptotic Bcl-2 with affinities comparable to those of Bcl-2's endogenous cellular counterparts. Structural studies revealed that FPV039 adopts the conserved Bcl-2 fold observed in cellular pro-survival Bcl-2 proteins, and closely mimics the structure of the pro-survival Bcl-2 family protein Mcl-1. Our findings suggest that FPV039 is a pan Bcl-2 protein inhibitor that can engage all host BH3-only proteins as well as Bcl-2 associated X, apoptosis regulator (Bax) and Bcl-2 antagonist/killer (Bak) proteins to inhibit premature apoptosis of an infected host cell. This work therefore provides a mechanistic platform to better understand FPV039-mediated apoptosis inhibition.

Journal article

Giotis ES, Robey RC, Skinner NG, Tomlinson CD, Goodbourn S, Skinner MAet al., 2016, Chicken interferome: avian interferon-stimulated genes identified by microarray and RNA-seq of primary chick embryo fibroblasts treated with a chicken type I interferon (IFN-α), Veterinary Research, Vol: 47, ISSN: 1297-9716

Viruses that infect birds pose major threats—to the global supply of chicken, the major, universally-acceptable meat, and as zoonotic agents (e.g. avian influenza viruses H5N1 and H7N9). Controlling these viruses in birds as well as understanding their emergence into, and transmission amongst, humans will require considerable ingenuity and understanding of how different species defend themselves. The type I interferon-coordinated response constitutes the major antiviral innate defence. Although interferon was discovered in chicken cells, details of the response, particularly the identity of hundreds of stimulated genes, are far better described in mammals. Viruses induce interferon-stimulated genes but they also regulate the expression of many hundreds of cellular metabolic and structural genes to facilitate their replication. This study focusses on the potentially anti-viral genes by identifying those induced just by interferon in primary chick embryo fibroblasts. Three transcriptomic technologies were exploited: RNA-seq, a classical 3′-biased chicken microarray and a high density, “sense target”, whole transcriptome chicken microarray, with each recognising 120–150 regulated genes (curated for duplication and incorrect assignment of some microarray probesets). Overall, the results are considered robust because 128 of the compiled, curated list of 193 regulated genes were detected by two, or more, of the technologies.

Journal article

Long J, Efstathios SG, Moncorge O, Frise R, Mistry B, James J, Morrison M, Iqbal M, Vignal A, Skinner MA, Barclay WSet al., 2016, Species difference in ANP32A underlies influenza A virus polymerase host restriction, Nature, Vol: 529, Pages: 101-104, ISSN: 1476-4687

Influenza pandemics occur unpredictably when zoonotic influenza viruses with novel antigenicity acquire the ability to transmit amongst humans1. Host range breaches are limited by incompatibilities between avian virus components and the human host. Barriers include receptor preference, virion stability and poor activity of the avian virus RNA-dependent RNA polymerase in human cells2. Mutants of the heterotrimeric viral polymerase components, particularly PB2 protein, are selected during mammalian adaptation, but their mode of action is unknown3, 4, 5, 6. We show that a species-specific difference in host protein ANP32A accounts for the suboptimal function of avian virus polymerase in mammalian cells. Avian ANP32A possesses an additional 33 amino acids between the leucine-rich repeats and carboxy-terminal low-complexity acidic region domains. In mammalian cells, avian ANP32A rescued the suboptimal function of avian virus polymerase to levels similar to mammalian-adapted polymerase. Deletion of the avian-specific sequence from chicken ANP32A abrogated this activity, whereas its insertion into human ANP32A, or closely related ANP32B, supported avian virus polymerase function. Substitutions, such as PB2(E627K), were rapidly selected upon infection of humans with avian H5N1 or H7N9 influenza viruses, adapting the viral polymerase for the shorter mammalian ANP32A. Thus ANP32A represents an essential host partner co-opted to support influenza virus replication and is a candidate host target for novel antivirals.

Journal article

Giotis ES, Robey RR, Ross C, Goodbourn SE, Skinner MAet al., 2015, Transcriptomic analysis of the chicken interferome, 3rd Annual Meeting of the International-Cytokine-and-Interferon-Society (ICIS), Publisher: Elsevier, Pages: 104-104, ISSN: 1043-4666

Conference paper

Crudgington B, Everett H, Skinner M, Crooke Het al., 2015, Investigation of Porcine Interferons as a metaphylactic intervention strategy against Classical Swine Fever Virus (CSFV), 3rd Annual Meeting of the International-Cytokine-and-Interferon-Society (ICIS), Publisher: Elsevier, Pages: 107-108, ISSN: 1043-4666

Conference paper

Giotis ES, Robey RR, Ross C, Laidlaw S, Goodbourn S, Skinner MAet al., 2015, Immunodulation and proviral action of chicken Suppressor of Cytokine Signaling 1 (SOCS1), 3rd Annual Meeting of the International-Cytokine-and-Interferon-Society (ICIS), Publisher: Elsevier, Pages: 90-90, ISSN: 1043-4666

Conference paper

Buttigieg KR, Skinner MA, 2015, Construction of FWPV Chimaeric MVA., Bio Protoc, Vol: 5, ISSN: 2331-8325

Construction of chimaeric MVA is a useful tool with which to study gene function of related viruses. The protocol given here describes MVA chimaeras containing genes from Fowlpox virus (FWPV), although this can be applied to DNA derived from other organisms. There are a number of steps required to make the chimaeric MVA: 1) Purification of viral particles; 2) Extraction of DNA from purified viral particles; 3) Assembly of linear recombination templates; 4) Transfection of linear recombination templates; 5) Selection of chimaeric MVA. Note: This procedure uses live virus, and should be conducted using Good Microbiological Practice, in accordance with international and national biocontainment requirements. This procedure also involves Genetic Modification of microorganisms, and appropriate safety approval should be obtained before commencing.

Journal article

Schmid M, Smith J, Burt DW, Aken BL, Antin PB, Archibald AL, Ashwell C, Blackshear PJ, Boschiero C, Brown CT, Burgess SC, Cheng HH, Chow W, Coble DJ, Cooksey A, Crooijmans RPMA, Damas J, Davis RVN, de Koning D-J, Delany ME, Derrien T, Desta TT, Dunn IC, Dunn M, Ellegren H, Eoery L, Erb I, Farre M, Fasold M, Fleming D, Flicek P, Fowler KE, Fresard L, Froman DP, Garceau V, Gardner PP, Gheyas AA, Griffin DK, Groenen MAM, Haaf T, Hanotte O, Hart A, Haesler J, Hedges SB, Hertel J, Howe K, Hubbard A, Hume DA, Kaiser P, Kedra D, Kemp SJ, Klopp C, Kniel KE, Kuo R, Lagarrigue S, Lamont SJ, Larkin DM, Lawal RA, Markland SM, McCarthy F, McCormack HA, McPherson MC, Motegi A, Muljo SA, Muensterberg A, Nag R, Nanda I, Neuberger M, Nitsche A, Notredame C, Noyes H, O'Connor R, O'Hare EA, Oler AJ, Ommeh SC, Pais H, Persia M, Pitel F, Preeyanon L, Barja PP, Pritchett EM, Rhoads DD, Robinson CM, Romanov MN, Rothschild M, Roux P-F, Schmidt CJ, Schneider A-S, Schwartz MG, Searle SM, Skinner MA, Smith CA, Stadler PF, Steeves TE, Steinlein C, Sun L, Takata M, Ulitsky I, Wang Q, Wang Y, Warren WC, Wood JMD, Wragg D, Zhou Het al., 2015, Third Report on Chicken Genes and Chromosomes 2015, CYTOGENETIC AND GENOME RESEARCH, Vol: 145, Pages: 78-179, ISSN: 1424-8581

Journal article

Ascough S, Sadeyen J-R, Giotis E, Laidlaw S, Staines K, Mwangi W, Hernandez RR, Skinner M, Butter Cet al., 2014, Potentiating the immunogenicity of poxvirus vectors to improve the efficacy of live recombinant viral vaccines in poultry, IMMUNOLOGY, Vol: 143, Pages: 66-66, ISSN: 0019-2805

Journal article

Laidlaw SM, Skinner MA, 2014, Construction of Deletion-knockout Mutant Fowlpox Virus (FWPV)., Bio Protoc, Vol: 4, ISSN: 2331-8325

The construction of deletion-knockout poxviruses is a useful approach to determining the function of specific virus genes. This protocol is an adaptation of the transient dominant knockout selection protocol published by Falkner and Moss (1990) for use with vaccinia virus. The protocol makes use of the dominant selectable marker Escherichia coli guanine phosphoribosyltransferase (gpt) gene (Mulligan and Berg, 1981), under the control of an early/late poxvirus promoter. The deletion viruses that are produced no longer contain a selectable marker, which may be preferable for the production of vaccines.

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

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

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

Book chapter

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

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

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

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

Schat KA, Skinner MA, 2008, Avian Immunosuppressive Diseases and Immune Evasion, Pages: 299-322

Journal article

Guzman E, Taylor G, Charleston B, Skinner MA, Ellis SAet al., 2008, An MHC-restricted CD8(+) 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

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

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

Book chapter

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://wlsprd.imperial.ac.uk:80/respub/WEB-INF/jsp/search-html.jsp Request URI: /respub/WEB-INF/jsp/search-html.jsp Query String: respub-action=search.html&id=00458693&limit=30&person=true