Imperial College London

DrEfstathiosGiotis

Faculty of MedicineDepartment of Medicine

Research Associate
 
 
 
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Contact

 

+44 (0)20 7594 9057e.giotis

 
 
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Location

 

Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

23 results found

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)., J Gen Virol

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

Tierney M, Gallagher AM, Giotis ES, Pentieva Ket al., 2017, An Online Survey on Consumer Knowledge and Understanding of Added Sugars, NUTRIENTS, Vol: 9, ISSN: 2072-6643

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-alpha), VETERINARY RESEARCH, Vol: 47, ISSN: 0928-4249

JOURNAL ARTICLE

Long JS, Giotis ES, Moncorgé O, Frise R, Mistry B, James J, Morisson 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: 0028-0836

© 2016 Macmillan Publishers Limited. All rights reserved. Influenza pandemics occur unpredictably when zoonotic influenza viruses with novel antigenicity acquire the ability to transmit amongst humans. 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 cells. Mutants of the heterotrimeric viral polymerase components, particularly PB2 protein, are selected during mammalian adaptation, but their mode of action is unknown. 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: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD, Pages: 104-104, 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: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD, Pages: 90-90, ISSN: 1043-4666

CONFERENCE PAPER

Giotis ES, Rothwell L, Scott A, Hu T, Talbot R, Todd D, Burt DW, Glass EJ, Kaiser Pet al., 2015, Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In Vivo Model., PLOS One, Vol: 10, Pages: e0134866-e0134866, ISSN: 1932-6203

Chicken Anaemia Virus (CAV) is an economically important virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected chickens at 14 dpi were also compared using a chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate <0.05) changes in expression in thymus and bone marrow on CAV infection were mainly associated with T-cell receptor signalling, immune response, transcriptional regulation, intracellular signalling and regulation of apoptosis. Expression levels of a number of adaptor proteins, such as src-like adaptor protein (SLA), a negative regulator of T-cell receptor signalling and the transcription factor Special AT-rich Binding Protein 1 (SATB1), were significantly down-regulated by CAV infection, suggesting potential roles for these genes as regulators of viral infection or cell def

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

Kennedy TG, Giotis ES, McKevitt AI, 2014, Microbial assessment of an upward and downward dehiding technique in a commercial beef processing plant, MEAT SCIENCE, Vol: 97, Pages: 486-489, ISSN: 0309-1740

JOURNAL ARTICLE

Wheatley P, Giotis ES, McKevitt AI, 2014, Effects of slaughtering operations on carcass contamination in an Irish pork production plant, IRISH VETERINARY JOURNAL, Vol: 67, ISSN: 0368-0762

JOURNAL ARTICLE

Laidlaw SM, Robey R, Davies M, Giotis ES, 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, Pages: 5041-5052, ISSN: 0022-538X

JOURNAL ARTICLE

Carson M, Meredith AL, Shaw DJ, Giotis ES, Lloyd DH, Loeffler Aet al., 2012, Foxes As a Potential Wildlife Reservoir for mecA-Positive Staphylococci, VECTOR-BORNE AND ZOONOTIC DISEASES, Vol: 12, Pages: 583-587, ISSN: 1530-3667

JOURNAL ARTICLE

Giotis ES, Loeffler A, Knight-Jones T, Lloyd DHet al., 2012, Development of a skin colonization model in gnotobiotic piglets for the study of the microbial ecology of meticillin-resistant Staphylococcus aureus ST398, JOURNAL OF APPLIED MICROBIOLOGY, Vol: 113, Pages: 992-1000, ISSN: 1364-5072

JOURNAL ARTICLE

Porphyre T, Giotis ES, Lloyd DH, Dorothea K, Staerk Cet al., 2012, A Metapopulation Model to Assess the Capacity of Spread of Meticillin-Resistant Staphylococcus aureus ST398 in Humans, PLOS ONE, Vol: 7, ISSN: 1932-6203

JOURNAL ARTICLE

Giotis ES, Loeffler A, Lindsay JA, Lloyd DHet al., 2011, Reduced Sensitivity of Oxacillin-Screening Agar for Detection of MRSA ST398 from Colonized Pigs, JOURNAL OF CLINICAL MICROBIOLOGY, Vol: 49, Pages: 3103-3104, ISSN: 0095-1137

JOURNAL ARTICLE

Giotis ES, Muthaiyan A, Natesan S, Wilkinson BJ, Blair IS, McDowell DAet al., 2010, Transcriptome Analysis of Alkali Shock and Alkali Adaptation in Listeria monocytogenes 10403S, FOODBORNE PATHOGENS AND DISEASE, Vol: 7, Pages: 1147-1157, ISSN: 1535-3141

JOURNAL ARTICLE

Krysa J, Zita J, Zlamal M, Kluson P, Giotis ES, Loeffler A, Stark KDC, Lloyd DAet al., 2010, Ability of Photocatalytic TiO2 Surfaces to Destroy MRSA ST398 under Controlled UV Light Conditions, 6th European Meeting on Solar Chemistry and Photocatalysis: Environmental Applications (SPEA6), Publisher: ICT PRESS, Pages: 333-333

CONFERENCE PAPER

Giotis ES, Julotok M, Wilkinson BJ, Blair IS, McDowell DAet al., 2008, Role of sigma B factor in the alkaline tolerance response of Listeria monocytogenes 10403S and cross-protection against subsequent ethanol and osmotic stress., J Food Prot, Vol: 71, Pages: 1481-1485, ISSN: 0362-028X

Many of the considerable abilities of Listeria monocytogenes to persist and grow in a wide range of adverse environmental conditions are thought to be at least partly under the control of the alternative sigma factor (sigmaB), encoded by the sigB gene. However, little is known about the role of this master regulon in the impressive ability of Listeria to persist and grow under conditions of alkaline pH. In this study, Northern blot analysis of parent Listeria mRNA revealed that alkali adaptation (pH 9.5 for 1 h) significantly increased the expression of sigB-derived mRNA. The study included a comparison of the relative survival of mid-exponential populations of adapted and nonadapted parent type (sigmaB expressing) and mutant (not sigmaB expressing, deltasigB) Listeria strains during subsequent alkaline (pH 12.0), osmotic (25% NaCl, wt/vol), or ethanol (16.5%) stress. Alkali-adapted parent strains were more resistant to pH 12.0 than were adapted deltasigB type strains, but both alkali-adapted parent and deltasigB strains were more resistant to pH 12.0 than were nonadapted strains. Alkali-adapted parent strains were more resistant to osmotic stress than were adapted deltasigB type strains. No significant differences in viability were observed between alkali-adapted parent and deltasigB strains after ethanol stress, suggesting that cross-protection against osmotic stress is mediated by sigmaB whereas cross-protection against ethanol is sigmaB independent. Overall, alkali-induced cross-protection against osmotic and ethanol challenges may have serious implications for food safety and human health because such stress conditions are routinely used as part of food preservation and surface cleaning processes.

JOURNAL ARTICLE

Giotis ES, Muthaiyan A, Blair IS, Wilkinson BJ, McDowell DAet al., 2008, Genomic and proteomic analysis of the Alkali-Tolerance Response (AlTR) in Listeria monocytogenes 10403S, BMC MICROBIOLOGY, Vol: 8, ISSN: 1471-2180

JOURNAL ARTICLE

Singh VK, Hattangady DS, Giotis ES, Singh AK, Chamberlain NR, Stuart MK, Wilkinson BJet al., 2008, Insertional inactivation of branched-chain alpha-keto acid dehydrogenase in Staphylococcus aureus leads to decreased branched-chain membrane fatty acid content and increased susceptibility to certain stresses, APPLIED AND ENVIRONMENTAL MICROBIOLOGY, Vol: 74, Pages: 5882-5890, ISSN: 0099-2240

JOURNAL ARTICLE

Giotis ES, Blair IS, McDowell DA, 2007, Morphological changes in Listeria monocytogenes subjected to sublethal alkaline stress, INTERNATIONAL JOURNAL OF FOOD MICROBIOLOGY, Vol: 120, Pages: 250-258, ISSN: 0168-1605

JOURNAL ARTICLE

Giotis ES, McDowell DA, Blair IS, Wilkinson BJet al., 2007, Role of branched-chain fatty acids in pH stress tolerance in Listeria monocytogenes, APPLIED AND ENVIRONMENTAL MICROBIOLOGY, Vol: 73, Pages: 997-1001, ISSN: 0099-2240

JOURNAL ARTICLE

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

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