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Dr Ceri Fielding

Dr Ceri Fielding

Research Fellow

School of Medicine

Email
fieldingca@cardiff.ac.uk
Telephone
+44 (0)2922 510233
Campuses
UG17, Henry Wellcome Building for Biomedical Research, University Hospital of Wales, Heath Park, Cardiff, CF14 4XN
Users
Available for postgraduate supervision

Overview

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.

Biography

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

Publications

2022

2021

2020

2018

2017

2016

2015

2014

2013

2012

2011

2010

2009

2008

2007

2006

2005

2004

2003

2001

Teaching

  • 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

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).

Supervision

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

Current supervision

Ms Pragati Sabberwal

Research student

Past projects

Co-supervisor (33%) for Pragati Sabberwal - Using CRISPR-Cas9 screens to investigate human cytomegalovirus infection

Supervisor (50%) for Hester Nichols - An analysis of human cytomegalovirus gene family function

Co-supervisor (33%) for Chantal Colmont

Co-supervisor (33%) for Tanya Bodenham

Engagement

  • British Society for Immunology ‘Celebrate Vaccines’ session at Swansea Science Festival 2020
  • Techniquest After hours ‘Rogue Cells’ (2020) representing the British Society for Immunology
  • Techniquest After hours ‘Superbugs’ (2018) representing the British Society for Immunology
  • ‘Science in Health’ open day ‘Innate Immunity’ tour 
  • ‘Science in Health’ work experience scheme
  • MedWales event
  • Kidney Wales Foundation open day
  • Leukaemia Research Fund open day