Dr Andrew Bell PhD BSc

Dr Andrew Bell

Institute of Cancer and Genomic Sciences
Research Fellow

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Institute of Cancer and Genomic Sciences

Dr Andrew Bell is a Research Fellow in the Institute of Cancer and Genomic Sciences. His research aims to understand how Epstein-Barr virus, a common herpesvirus with oncogenic properties, contributes to the development of several human malignancies. This work is funded by Cancer Research UK and involves collaborations with other members of the Centre for Human Virology

Qualifications

  • PhD in Biochemistry, University of Birmingham 1990
  • BSc (Hons) in Biochemistry, 1987

Teaching

  • BSc Biomedical Science
  • MBChB Cancer: Causes to Cures
  • B Med Sci Clinical Sciences (Intercalated)
  • MSc/PGDip Clinical Oncology
  • MSc Genomic Medicine

Postgraduate supervision

Dr Bell is happy to discuss opportunities to undertake research on Epstein-Barr virus or its associated diseases.

Research

The main aim of Dr Bell’s research is to understand how infection with the Epstein-Barr virus (EBV) is linked to the development of several human cancers. In collaboration with colleagues in the Institute of Cancer and Genomic Sciences, Institute of  Immunology and Immunotherapy and Centre for Human Virology, Dr Bell’s research focusses on the following areas:

EBV infection in healthy individuals

EBV establishes a persistent asymptomatic infection in the B cell system. We are interested in understanding how EBV exploits the natural process of B cell differentiation to gain access to the long-lived memory B cell pool while evading the host immune system.

EBV-driven B cell transformation

A clue to EBV’s role in lymphoma development comes from the observation that EBV can transform normal B lymphocytes in vitro into continuously growing lymphoblastoid cells. Our work aims to understand how different viral genes contribute to this growth transformation process and identify virus-induced cellular changes that might be relevant to EBV-associated diseases.

EBV-associated B cell lymphomas

EBV is linked to a remarkable range of malignancies of B cell and epithelial cell origin. We are particularly interested in how EBV contributes to the development of four B cell lymphomas: post- transplant lymphoproliferative disease, diffuse large B cell lymphoma, Hodgkin lymphoma and Burkitt lymphoma. 

Other activities

  • EBV Association Board member (2012-)
  • Member of Microbiology Society

Publications

Woon HG, Braun A, Li J, Smith C, Edwards J, Sierro F, Feng CG, Khanna R, Elliot M, Bell A, Hislop AD, Tangye SG, Rickinson AB, Gebhardt T, Britton WJ, Palendira U (2016). Compartmentalization of total and virus-specific tissue-resident memory CD8+ T Cells in human lymphoid organs. PLoS Pathog 12(8): e1005799.

Nicol SM, Sabbah S, Brulois KF, Jung JU, Bell AI, Hislop AD (2016). Primary B lymphocytes infected with KSHV can be expanded in vitro and are recognized by LANA-specific CD4+ T cells. J Virol 90(8):3849-59. 

Burns DM, Rana S, Martin E, Nagra S, Ward J, Osman H, Bell AI, Moss P, Russell NH, Craddock CF, Fox CP, Chaganti S (2016). Greatly reduced risk of EBV reactivation in rituximab-experienced recipients of alemtuzumab-conditioned allogeneic HSCT. BMT Feb 22. doi: 10.1038/bmt.2016.19.  [Epub ahead of print]

Murray P, Bell A (2015) Contribution of the Epstein-Barr virus to the pathogenesis of Hodgkin lymphoma. Curr Top Microbiol Immunol 390 (1): 287-313. doi: 10.1007/978-3-319-22822-8_12.

Burns DM, Tierney R, Shannon-Lowe C, Croudace J, Inman C, Abbotts B, Nagra S, Fox CP, Chaganti S, Craddock C, Moss P, Rickinson AB, Rowe M and Bell AI (2015). Memory B cell reconstitution following allogeneic haematopoietic stem cell transplantation is an EBV-associated transformation event.  Blood 126(25):2665-75. doi: 10.1182/blood-2015-08-665000. Epub 2015 Oct 8. 

Jayasooriya S, de Silva TI, Njie-Jobe J, Sanyang C, Leese AM, Bell AI, McAulay KA, Yanchun P, Long HM, Dong T, Whittle HC, Rickinson AB, Rowland-Jones, SL, Hislop AD and Flanagan KL (2015).Early virological and immunological events in asymptomatic Epstein-Barr virus infection in African children. PLoS Pathog 11(3):e1004746.

Tierney RJ, Nagra J, Rowe M, Bell AI and Rickinson AB (2015). The Epstein-Barr virus BamHI C promoter is not essential for B cell immortalisation in vitro but greatly enhances B cell growth transformation. J Virol 89: 2483-2493.

Tierney RJ, Shannon-Lowe C, Fitzsimmons L, Bell AI and Rowe M. Unexpected patterns of Epstein-Barr virus transcription revealed by a high throughput PCR array for absolute quantification of viral mRNA. (2015) Virology 474: 117-130.

Kelly GL, Stylianou J, Rasaiyaah J, Wei W, Thomas W, Croom-Carter D, Kohler C, Spang R, Woodman C, Kellam P, Rickinson AB, Bell AI. (2013). Different patterns of Epstein-Barr virus latency in endemic Burkitt lymphoma (BL) lead to distinct variants within the BL-associated gene expression signature. J Virol 87:2882-94.

Heath, E, Begue-Pastor, N, Chaganti,S, Croom-Carter, D, Shannon-Lowe, C, Kube, D, Feederle, R, Delecluse, HJ, Rickinson, ABand Bell, AI (2012). Epstein-Barr virus infection of naïve B cells in vitro frequently selects clones with mutated immunoglobulin genotypes: implications for virus biology. PLoS Pathog. 8(5): e1002697. doi:10.1371/journal.ppat.1002697

Jayasooriya S, Hislop A, Peng Y, Croom-Carter D, Jankey Y, Bell, A, Dong, T, Rowland-Jones, S, Rickinson, A, Walther, M and Whittle, H (2012). Revisiting the effect of acute P. falciparum malaria on Epstein-Barr virus: Host balance in the setting of reduced malaria endemicity. PLoS ONE 7(2): e31142. doi:10.1371/journal.pone.0031142

Amoroso, R, Fitzsimmons, L, Thomas, WA, Kelly, GL, Rowe, M and Bell, AI (2011). Quantitative studies of Epstein-Barr virus-encoded microRNAs provide novel insights into their regulation. J. Virol. 85: 996-1010.