Dr Claire Shannon-Lowe

Claire Shannon-Lowe

Institute of Immunology and Immunotherapy
Virology Lecturer

Contact details

Telephone
+44 (0)121 414 6425
Email
c.shannonlowe@bham.ac.uk
View my research portal
Address
Institute of Immunology and Immunotherapy
College of Medical and Dental Sciences
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

Claire Shannon-Lowe is a lecturer in virology at the Institute of Immunology and Immunotherapy.

Claire’s research primarily focuses on three key areas: The mechanism of Epstein Barr virus (EBV) entry into epithelial cells, T cells and Natural Killer cells; How EBV contributes to cancer development of these cell types; How EBV contributes to resistance to chemotherapy in these cancers. This work is currently funded by the MRC. 

Qualifications

  • PhD in Virology 2002, The Royal Free and University College Hospital
  • MSc in Medical Microbiology 1997, The University of Surrey
  • BSc Hons (2:1) in Applied Biology 1993

Biography

Claire Shannon-Lowe studied for a PhD in Virology at The Royal Free and University College Medical School in London where she worked on Cytomegalovirus resistance to antivirals in AIDS patients. She then went on to post doctoral research at the Cancer Research UK Institute for Cancer Studies at The University of Birmingham with Professors Henri-Jacques Delecluse, Alan Rickinson and Martin Rowe. In 2011 Claire was awarded a MRC New Investigator Award.

Claire Shannon-Lowe’s research has focused on the mechanisms of Epstein Barr virus (EBV) entry into EBV-receptor deficient cells including epithelial cells and lymphocytes (T- and NK cells) where EBV infection is associated with malignancies of epithelial, T- and NK cell lineages, including nasopharyngeal and gastric carcinoma, haemophagocytic lymphohistiocytosis, NK leukaemia, extranodal NK/T cell lymphoma.

Claire’s laboratory previously identified how EBV efficiently infects epithelial cells and demonstrated a physiological role for this mode of entry. She has also recently identified the route of entry into T cells and NK cells, previously thought to be refractory to infection. Her laboratory is now concentrating on the events immediately following infection and subsequent development of the associated diseases.

Teaching

Postgraduate supervision

Claire has supervised PhD students, Masters by Research students and intercalating BSc students.

Claire is interested in supervising doctoral research students in the following areas:      

  • The role of EBV in T and NK cell maliganacies.                        
  • The role of EBV in gastric carcinoma.

If you are interested in studying any of these subject areas please contact Claire, or for any general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 6425.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research Programme listings.

Research

Epstein Barr virus infects the majority of the human population and establishes a silent ‘latent’ infection in B cells. In order for the virus to spread between individuals, it also infects oral epithelial cells where the virus is replicated and shed into saliva. However, on rare occasions the virus infects T cells and NK cells where it causes a range of diseases, from lymphoproliferations to aggressive malignancies. These diseases are often resistant to chemotherapy and the disease outcomes are usually poor. Claire’s laboratory is interested in how EBV infects T cells and NK cells, how EBV causes the range of diseases and how EBV contributes to the chemotherapy resistance with a view to finding alternative effective treatment strategies.

Claire’s group currently runs a large UK-wide study to identify patients with EBV-associated T/NK cell diseases including Haemophagocytic Lymphohistiocytosis, Chronic Active EBV, Extranodal NK/T cell lymphoma and Aggressive NK leukaemia. The EBV-infected lymphocytes are identified, phenotyped, purified and cultured then examined for susceptibility to a range of novel drugs to identify effective chemotherapeutic drugs for these difficult to treat diseases.

EBV is associated with approximately 10% of gastric carcinoma worldwide, accounting for up to 80,000 deaths per year. EBV-associated gastric carcinoma are genetically distinct from all other subtypes of gastric carcinoma, yet very little is know about how EBV even infects the gastric epithelial cells. Claire’s laboratory is currently investigating how EBV causes gastric carcinoma and has recently established a new physiologically relevant primary epithelial cell culture system to examine how EBV triggers the changes in the gastric epithelial cells leading to gastric carcinoma.

Other activities

Memberships:

Society for General Microbiology.

Peer Reviewing:

Reviewer of manuscripts submitted to several virology and cell biology journals.
Reviewer for grant funding bodies including Kay Kendal Research Fund and Worldwide Cancer Research.

External examination:

External PhD examiner in the areas of Epstein Barr virus.

Publications

Burns D, Tierney RJ, Shannon-Lowe C, Croudace J, Inman C, Abbotts B, Nagra S, Fox CP, Chaganti S, Craddock C, Moss P, Rickinson A, Rowe M. Memory B cell reconstitution following allogeneic haematopoietic stem cell transplantation is an EBV-associated transformation event. 2015. Blood (Under review).

Tierney RJ, Shannon-Lowe CD, Fitzsimmons L, Bell AI, Rowe M. Unexpected patterns of Epstein-Barr virus transcription revealed by a high throughput PCR array for absolute quantification of viral mRNA. Virology. 2015; 474:117-30.

Vockerodt M, Cader FZ, Shannon-Lowe C, Murray P. Epstein-Barr virus and the origin of Hodgkin lymphoma. Chin J Cancer. 2014; 33(12):591-7.

Vockerodt M, Yap LF, Shannon-Lowe C, Curley H, Wei W, Vrzalikova K, Murray PG. The Epstein-Barr virus and the pathogenesis of lymphoma. J Pathol. 2015; 235(2):312-22.

Vento-Tormo R, Rodríguez-Ubreva J, Lisio LD, Islam AB, Urquiza JM, Hernando H, López-Bigas N, Shannon-Lowe C, Martínez N, Montes-Moreno S, Piris MA, Ballestar E. NF-κB directly mediates epigenetic deregulation of common microRNAs in Epstein-Barr virus-mediated transformation of B-cells and in lymphomas. Nucleic Acids Res. 2014; 42(17):11025-39.

Martin Rowe,Sweta Raithatha and Claire Shannon-Lowe. Counteracting effects of cellular Notch and Epstein-Barr virus EBNA2: implications for stromal effects on virus-host interactions. J Virol. 2014; 88(20):12065-76.

Quinn L, Zuo J, Abbott R, Shannon-Lowe C, Tierney R, Hislop A, Rowe M. Cooperation between Epstein-Barr virus immune evasion proteins spreads protection from CD8+ T cell recognition across all three phases of the lytic cycle. PLoS Pathogens. 2014:10(8):e1004322

Claire Shannon-Lowe and Martin Rowe. Epstein Barr virus entry: Kissing and conjugation. Curr Opin Virol 2014 Feb:4:78-84

Hernando H, Islam AB, Rodríguez-Ubreva J, Forné I, Ciudad L, Imhof A, Shannon-Lowe C, Ballestar E. Epstein-Barr virus-mediated transformation of B cells induces global chromatin changes independent to the acquisition of proliferation. Nucleic Acids Research. 2014 42(1):249-63

Hernando H, Shannon-Lowe C, Islam AB, Al-Shahrour F, Rodríguez-Ubreva J, Rodríguez-Cortez VC, Javierre BM, Mangas C, Fernández AF, Parra M, Delecluse HJ, Esteller M, López-Granados E, Fraga MF, López-Bigas N, Ballestar E. The B cell transcription program mediates hypomethylation and overexpression of key genes in Epstein-Barr virus-associated proliferative conversion. Genome Biol 2013:14(1):R3

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

Fox CP, Shannon-Lowe C, Rowe M. Deciphering the role of Epstein Barr virus in the pathogenesis of T and NK cell lymphoproliferations. Herpesviridae. 2011 Sep 7;2:8.

Shannon-Lowe C and Rowe M. Epstein-Barr virus infection of polarized epithelial cells via the basolateral surface by memory B cell-mediated transfer infection. PLoS Pathogens 2011 May;7(5):e1001338.

Heather M. Long, Alison M. Leese, Odette L. Chagoury, Shawn R. Connerty, Jared Quarcoopome, Laura L. Quinn, Claire Shannon-Lowe, Alan B. Rickinson. Cytotoxic CD4+ T cell responses to Epstein-Barr virus contrast with CD8 responses in breadth of lytic cycle antigen choice and in lytic cycle recognition. J.Immunol 2011 Jul 1;187(1):92-101.

Shannon-Lowe C, Emery VC. The effects of maribavir on the autophosphorylation of ganciclovir resistant mutants of the cytomegalovirus UL97 protein. Herpesviridae. 2010 Dec 7;1(1):4.

Fox CP, Haigh TA, Taylor GS, Long HM, Lee SP, Shannon-Lowe C, O'Connor S, Bollard CM, Iqbal J, Chan WC, Rickinson AB, Bell AI, Rowe M. A novel latent membrane 2 transcript expressed in Epstein-Barr virus-positive NK and T cell lymphoproliferative disease encodes a target for cellular immunotherapy. Blood. 2010 Nov 11;116(19):3695-704.

Fox CP, Shannon-Lowe C, Gothard P, Kishore B, Neilson J, O'Connor N, Rowe M. Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis in adults characterized by high viral genome load within circulating natural killer cells. Clin Infect Dis. 2010 Jul 1;51(1):66-9.

Shannon-Lowe C, Adland E, Bell AI, Delecluse HJ, Rickinson AB, Rowe M. Features distinguishing Epstein-Barr virus infections of epithelial cells and B cells: viral genome expression, genome maintenance, and genome amplification. J Virol. 2009 Aug;83(15):7749-60

Croft NP, Shannon-Lowe C, Bell AI, Horst D, Kremmer E, Ressing ME, Wiertz EJ, Middeldorp JM, Rowe M, Rickinson AB, Hislop AD. Stage-specific inhibition of MHC class I presentation by the Epstein-Barr virus BNLF2a protein during virus lytic cycle. PLoS Pathog. 2009 Jun;5(6):e1000490

Zuo J, Currin A, Griffin BD, Shannon-Lowe C, Thomas WA, Ressing ME, Wiertz EJ, Rowe M. The Epstein-Barr virus G-protein-coupled receptor contributes to immune evasion by targeting MHC class I molecules for degradation. PLoS Pathog. 2009 Jan;5(1):e1000255.

Stamataki Z, Shannon-Lowe C, Shaw J, Mutimer D, Rickinson AB, Gordon J, Adams DH, Balfe P, McKeating JA. Hepatitis C virus association with peripheral blood B lymphocytes potentiates viral infection of liver-derived hepatoma cells. Blood. 2009 Jan 15;113(3):585-93.  

Tierney R, Nagra J, Hutchings I, Shannon-Lowe C, Altmann M, Hammerschmidt W, Rickinson A, Bell A. Epstein-Barr virus exploits BSAP/Pax5 to achieve the B-cell specificity of its growth-transforming program. J Virol. 2007 Sep;81(18):10092-100.

Feederle R, Neuhierl B, Bannert H, Geletneky K, Shannon-Lowe C, Delecluse HJ. Epstein-Barr virus B95.8 produced in 293 cells shows marked tropism for differentiated primary epithelial cells and reveals interindividual variation in susceptibility to viral infection. Int J Cancer. 2007 Aug 1;121(3):588-94.

Shannon-Lowe CD, Neuhierl B, Baldwin G, Rickinson AB, Delecluse HJ. Resting B cells as a transfer vehicle for Epstein-Barr virus infection of epithelial cells. Proc Natl Acad Sci U S A. 2006 May 2;103(18):7065-70.

Shannon-Lowe C, Baldwin G, Feederle R, Bell A, Rickinson A, Delecluse HJ. Epstein-Barr virus-induced B-cell transformation: quantitating events from virus binding to cell outgrowth. J Gen Virol. 2005 Nov;86(Pt 11):3009-19.

Feederle R, Shannon-Lowe C, Baldwin G, Delecluse HJ. Defective infectious particles and rare packaged genomes produced by cells carrying terminal-repeat-negative Epstein-Barr virus. J Virol. 2005 Jun;79(12):7641-7.

Bar M, Shannon-Lowe C, Geballe AP. Differentiation of human cytomegalovirus genotypes in immunocompromised patients on the basis of UL4 gene polymorphisms. J Infect Dis. 2001 Jan 15;183(2):218-225.

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