Dr Ceri Fielding

Lecturer

: Available for postgraduate supervision

I'm a Lecturer in Virology within the 'Viral Immunology' group and also the 'Cytomegalovirus and Adenovirus Virology' group. My research investigates the interaction of viruses with the human immune system. Previously I've studied immune interactions with cytomegalovirus, the major infectious cause of birth defects and a problem in transplant patients, and SARS-CoV-2, the cause of COVID-19. I'm now also looking at how RNA viruses with pandemic potential interact with the innate immune system.

Date
Type

2015

Wilkinson, G. W. G. et al. 2015. Human cytomegalovirus: taking the strain. Medical Microbiology and Immunology 204(3), pp. 273-284. (10.1007/s00430-015-0411-4)
Fielding, C. A. 2015. Mimicry of cytokine pathways by human herpesviruses. Future Virology 10(1), pp. 41-51. (10.2217/fvl.14.101)

2014

Weekes, M. et al. 2014. Quantitative temporal viromics: an approach to investigate host-pathogen interaction. Cell 157(6), pp. 1460-1472. (10.1016/j.cell.2014.04.028)
Fielding, C. A. et al. 2014. Two novel human cytomegalovirus NK cell evasion functions target MICA for lysosomal degradation. PLoS Pathogens 10(5), article number: e1004058. (10.1371/journal.ppat.1004058)
Jones, S. A., Fraser, D. J., Fielding, C. A. and Jones, G. W. 2014. Interleukin-6 in renal disease and therapy. Nephrology Dialysis Transplantation 30(4), pp. 564-574. (10.1093/ndt/gfu233)
Seirafian, S., Prod'homme, V., Sugrue, D., Davies, J., Fielding, C., Tomasec, P. and Wilkinson, G. W. G. 2014. Human cytomegalovirus suppresses Fas expression and function. Journal of General Virology 95(4), pp. 933-939. (10.1099/vir.0.058313-0)
Fielding, C. A. et al. 2014. Interleukin-6 signaling drives fibrosis in unresolved inflammation. Immunity 40(1), pp. 40-50. (10.1016/j.immuni.2013.10.022)

2013

Lauder, S. N. et al. 2013. Interleukin-6 limits influenza-induced inflammation and protects against fatal lung pathology. European Journal of Immunology 43(10), pp. 2613-2625. (10.1002/eji.201243018)
Fielding, C. A., Jones, G. W., Taylor, P. R., Jenkins, B. J., Topley, N. and Jones, S. A. 2013. IL-6 regulation of Th1 responses drives fibrosis in unresolved inflammation [Abstract]. Cytokine 63(3), pp. 262. (10.1016/j.cyto.2013.06.082)

2012

Pembroke, T. et al. 2012. Rapid early innate control of hepatitis C virus during IFN-α treatment compromises adaptive CD4+T-cell immunity. European Journal of Immunology 42(9), pp. 2383-2394. (10.1002/eji.201142072)
Fielding, C. A. et al. 2012. A novel human cytomegalovirus gene function targets the natural killer cell activating ligand MICA for lysosomal degradation [Abstract]. Immunology 137(S1), pp. 154. (10.1111/imm.12001)
Fielding, C. A. 2012. Interleukin-19: a new target to aim for?. Rheumatology 51(3), pp. 399-400. (10.1093/rheumatology/ker174)

2011

Colmont, C. S. et al. 2011. Human peritoneal mesothelial cells respond to bacterial ligands through a specific subset of Toll-like receptors. Nephrology Dialysis Transplantation 26(12), pp. 4079-4090. (10.1093/ndt/gfr217)

2010

Stumhofer, J. S. et al. 2010. A role for IL-27p28 as an antagonist of gp130-mediated signaling. Nature Immunology 11(12), pp. 1119-1126. (10.1038/ni.1957)
Lauder, S. N., Smart, K., Ondondo, B., Fielding, C. A., Godkin, A. J., Jones, S. A. and Gallimore, A. M. 2010. A critical role for interleukin-6 in limiting influenza-induced pathology and generating heterosubtypic immunity [Abstract]. Immunology 131(S1), pp. 186. (10.1111/j.1365-2567.2010.03390.x)
Lin, C. et al. 2010. The HMB-PP producing capacity of the causative pathogen and local gamma delta T cell numbers predict clinical outcome from bacterial peritonitis. Immunology 131, pp. 81-82.
Coles, B., Colmont, C. S., Fielding, C. A., Kift-Morgan, A., Hams, E., Topley, N. and Jones, S. A. 2010. Local manipulation of IL-6 trans-signaling therapeutically enhances anti-microbial host defense [Abstract]. Cytokine 52(1-2), pp. 80-81. (10.1016/j.cyto.2010.07.335)
Li, N., McLaren, J. E., Michael, D. R., Clement, M., Fielding, C. A. and Ramji, D. P. 2010. ERK is integral to the IFN-γ-mediated activation of STAT1, the expression of key genes implicated in atherosclerosis, and the uptake of modified lipoproteins by human macrophages. The Journal of Immunology 185(5), pp. 3041-3048. (10.4049/jimmunol.1000993)

2009

Luo, D. D., Fielding, C. A., Phillips, A. O. and Fraser, D. J. 2009. Interleukin-1 beta regulates proximal tubular cell transforming growth factor beta-1 signalling. Nephrology Dialysis Transplantation 24(9), pp. 2655-2665. (10.1093/ndt/gfp208)

2008

Jenkins, B. J. et al. 2008. Differential roles of IL-6 and IL-11 in inflammation and tumorigenesis [Abstract]. Cytokine 43(3), pp. 243-243. (10.1016/j.cyto.2008.07.069)
Rabe, B. et al. 2008. The role of IL6-transsignaling in acute and chronic inflammation [Abstract]. Cytokine 43(3), pp. 244-244. (10.1016/j.cyto.2008.07.073)
Hams, E. et al. 2008. Oncostatin M receptor-β signaling limits monocytic cell recruitment in acute inflammation. Journal of Immunology 181(3), pp. 2174-2180.
Fielding, C. A. et al. 2008. IL-6 regulates neutrophil trafficking during acute inflammation via STAT3. Journal of Immunology 181(3), pp. 2189-2195.
Hams, E. et al. 2008. Oncostatin M receptor-beta signaling limits monocytic cell recruitment in acute inflammation. Journal of Immunology 181(3), pp. 2174-2180.
Fielding, C. A. and Topley, N. 2008. Piece by piece: solving the puzzle of peritoneal fibrosis [Commentary]. Peritoneal Dialysis International 28(5), pp. 477-479.

2007

Chalaris, A. et al. 2007. Apoptosis is a natural stimulus of IL6R shedding and contributes to the proinflammatory trans-signaling function of neutrophils. Blood -New York- 110(6), pp. 1748-1755. (10.1182/blood-2007-01-067918)
Coles, B., Fielding, C. A., Rose-John, S., Scheller, J., Jones, S. A. and O'Donnell, V. B. 2007. Classic interleukin-6 receptor signaling and interleukin-6 trans-signaling differentially control angiotensin II-dependent hypertension, cardiac signal transducer and activator of transcription-3 activation, and vascular hypertrophy in vivo. American Journal of Pathology 171(1), pp. 315-325. (10.2353/ajpath.2007.061078)
Rabe, B. et al. 2007. IL6/sIL6R-transsignaling controls innate and aquired immunity [Abstract]. Cytokine 39(1), pp. 34-34. (10.1016/j.cyto.2007.07.129)
Hams, E. et al. 2007. Oncostatin M receptor signalling regulates monocytic cell trafficking during acute inflammation [Abstract]. Cytokine 39(1), pp. 14-14. (10.1016/j.cyto.2007.07.053)

2006

Nowell, M. A. et al. 2006. Regulation of pre-B cell colony-enhancing factor by STAT-3-dependent interleukin-6 trans-signaling: implications in the pathogenesis of rheumatoid arthritis. Arthritis & Rheumatism 54(7), pp. 2084-2095. (10.1002/art.21942)
Monslow, J. et al. 2006. Sp1 and Sp3 mediate constitutive transcription of the human hyaluronan synthase 2 gene. The Journal of Biological Chemistry 281(26), pp. 18043-18050. (10.1074/jbc.M510467200)
Osborne, C. S., Leitner, I., Hofbauer, B., Fielding, C. A., Favre, B. and Ryder, N. S. 2006. Biological, biochemical, and molecular characterization of a new clinical Trichophyton rubrum isolate resistant to terbinafine. Antimicrobial Agents and Chemotherapy 50(6), pp. 2234-2236. (10.1128/AAC.01600-05)
Richards, P. J. et al. 2006. Functional characterization of a soluble gp130 isoform and its therapeutic capacity in an experimental model of inflammatory arthritis. Arthritis & Rheumatism 54(5), pp. 1662-1672. (10.1002/art.21818)

2005

Fielding, C. A. et al. 2005. Viral IL-6 blocks neutrophil infiltration during acute inflammation. The Journal of Immunology 175(6), pp. 4024-4029.
Siebert, S., Fielding, C. A., Williams, B. D. and Brennan, P. 2005. Mutation of the extracellular domain of tumour necrosis factor receptor 1 causes reduced NF‐κB activation due to decreased surface expression. FEBS Letters 579(23), pp. 5193-5198. (10.1016/j.febslet.2005.08.037)
McLoughlin, R. M. et al. 2005. IL-6 trans-signaling via STAT3 directs T cell infiltration in acute inflammation. Proceedings of the National Academy of Sciences of the United States of America (PNAS) ISSN 1091-6490 102(27), pp. 9589-9594. (10.1073/pnas.0501794102)
Siebert, S., Amos, N., Fielding, C. A., Wang, E. C. Y., Aksentijevich, I., Williams, B. D. and Brennan, P. 2005. Reduced tumor necrosis factor signaling in primary human fibroblasts containing a tumor necrosis factor receptor superfamily 1A mutant. Arthritis & Rheumatism 52(4), pp. 1287-1282. (10.1002/art.20955)

2004

Fielding, C. A., Siebert, S., Rowe, M. and Brennan, P. 2004. Analysis of human tumour necrosis factor receptor 1 dominant-negative mutants reveals a major region controlling cell surface expression. FEBS Letters 570(1-3), pp. 138-142. (10.1016/j.febslet.2004.06.035)

2003

Richardson, C. J., Fielding, C., Rowe, M. and Brennan, P. 2003. Epstein-Barr virus regulates STAT1 through latent membrane protein 1. Journal of Virology 77(7), pp. 4439-4443. (10.1128/JVI.77.7.4439-4443.2003)

2001

Fielding, C. A., Sandvej, K., Mehl, A. M., Brennan, P., Jones, M. and Rowe, M. 2001. Epstein-Barr virus LMP-1 natural sequence variants differ in their potential to activate cellular signaling pathways. Journal of Virology 75(19), pp. 9129-9141. (10.1128/JVI.75.19.9129-9141.2001)

SARS-CoV-2

SARS-CoV-2 is the novel coronavirus, which causes COVID-19. Our recent findings have identified a mechanism by which SARS-CoV-2 is able to prevent activation of natural killer (NK) cells, a type of immune cell, by preventing the production of proteins ('activating ligands') which would activate them. It appears to do this by preventing their translation. This inhibition of NK cells can be overcome by SARS-CoV-2-specific antibodies present in people who have recovered from COVID-19. These antibodies recognise several different SARS-CoV-2 proteins present on the surface of the infected cell, including Spike (S), Nucleocapsid (N), Membrane (M) and Orf3a ( Fielding et al., 2022, https://doi.org/10.7554/eLife.74489).

Cytomegalovirus

Worldwide, most people are infected with cytomegalovirus (CMV) without realising it. CMV is closely related to herpes simplex, the virus that causes cold sores. Like herpes simplex, CMV infections are for life and must be constantly controlled by our immune system. Disease occurs when this control breaks down. CMV disease is a major problem in hospitals; primarily due to its capacity to cause life-threatening infections in immunosuppressed patients, particularly bone marrow, kidney and heart transplant recipients plus patients with HIV-AIDS. CMV disease can manifest in virtually any organs (e.g. lungs, intestine, lung, brain, eye, ear). Critically, CMV is able to cross the placenta to infect the foetus, and does so in ~1% of pregnancies. Congenital infection can induce miscarriage, is a common cause of deafness and in its more severe form causes brain damage. In brutal terms, the cost in patient care alone is $1.86 billion per year in the US. Congenital CMV disease is driving vaccine development. More subtly, CMV infection alters the make up of immune cells of apparently healthy carriers and the implications of this are not known. CMV is a major human pathogen that needs to be researched and merits a much higher public profile.

CMV is the most complex human virus containing nearly 200 genes, of which >124 genes are not required to replicate the virus. Research by us, and others, show many are controlling our immune system. As most of us carry this pathogen throughout life, it is important to find out what these genes are doing. To address this issue we first defined the genome of the clinical agent and then developed systems to screen for CMV gene function: we generated i) a vector library capable of expressing all CMV genes in cells individually and ii) a panel of CMV viruses deleted in large blocks of genes. Combining these resources has enabled us to rapidly map a substantial number of CMV immune evasion functions. However, we would also wanted to know how they worked. Collaborations have been established with researchers in Harvard and Cambridge to exploit state-of the-art proteomic systems to track expression of >700 cell surface and >7000 intracellular proteins during virus infections. These technologies combine to reveal exactly how individual CMV immune evasion genes act.

Natural Killer (NK) cells are white blood cells critical in controlling cytomegalovirus CMV disease. We are currently systematically screening all CMV genes for their capacity to modulate NK cell function. The CMV genome is organised into 'families' of related genes that have arisen by duplication of a common ancient precursor. Our current research aims to characterise the impact of two CMV gene families (the US12 family and the RL11 family) on the immune response to CMV, in particular of NK cells. Our recent work highlights the role of the US12 family in regulating NK cell function (Fielding et al., 2014, https://doi.org/10.1371/journal.ppat.1004058; Fielding et al., 2017, https://doi.org/10.7554/eLife.22206).

Tutor for Literature Review SSC 1st Year MBCH
Tutor for Virology tutorials 2nd Year MBCH
Lecturer and Assessor for ME3045 Advance Immunology module 3rd Year Pharmacology BSc and Intercalated Pathology; 'Interaction of viruses with the immune system' and 'Immune evasion by viruses'
Lecturer for Applied, Experimental and Clinical Immunology MSc; 'Antivirals' and 'COVID-19 pathogenesis'
Supervisor and Assessor for Pharmacology BSc laboratory projects
PhD student supervisor

Career Overview

2021-Present: Lecturer in Virology (HEFCW)
2011-2021: Post-doctoral Researcher, Cardiff University (3x MRC project grant, 1x Wellcome Trust Collaborative grant)
2009-2010: Value in People Award (Wellcome Trust)
2006-2009: Kidney Research UK Career Development Fellow
2003-2006: Post-doctoral Researcher, Cardiff University (Wellcome Trust)
2001-2003: Post-doctoral Researcher, University of Wales College of Medicine (Leverhulme Trust)

Education and Qualifications

1998-2001: PhD Molecular Virology, University of Wales College of Medicine (Leukaemia Research Fund)
1998-1999: Diploma in Biomedical Methods, University of Wales College of Medicine
1994-1998: BSc (Hons) with Intercalated Year Virology, University of Warwick

Honours and awards

Abstract Award, Renal Association conference (2010)
Sheldon Wolff Prize for Cytokine Research, International Cytokine Society (2004)

Professional memberships

Microbiology Society
British Society of Immunology

Committees and reviewing

Welsh Representative, Forum Committee, British Society of Immunology
Treasurer, South Wales Regional Group of British Society of Immunology

I am interested in supervising research projects for Biochemistry/Pharmacology/Medical Pharmacology BSc students (final year projects), professional training year (PTY) students, MSc student and PhD students in the areas of:

Virology
Immunology

Contact Details

FieldingCA@cardiff.ac.uk
+44 29225 10233
Henry Wellcome Building for Biomedical Research, Room UG17, University Hospital of Wales, Heath Park, Cardiff, CF14 4XN

Scientists shed new light on how SARS-CoV-2 evades the immune response in early infection

18 July 2022

New insight into leading viral cause of congenital birth defects

04 April 2017

Dr Ceri Fielding

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