Andrew Bell

ORCID: 0000-0001-9520-4417
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About
Contact & Profiles
Research Areas
  • Viral-associated cancers and disorders
  • Lymphoma Diagnosis and Treatment
  • Immune Cell Function and Interaction
  • Parvovirus B19 Infection Studies
  • Cytomegalovirus and herpesvirus research
  • Bacterial Genetics and Biotechnology
  • Eosinophilic Disorders and Syndromes
  • Histiocytic Disorders and Treatments
  • RNA and protein synthesis mechanisms
  • Polyomavirus and related diseases
  • Health Sciences Research and Education
  • Chronic Lymphocytic Leukemia Research
  • DNA and Nucleic Acid Chemistry
  • Genomics and Chromatin Dynamics
  • T-cell and B-cell Immunology
  • Systemic Sclerosis and Related Diseases
  • CNS Lymphoma Diagnosis and Treatment
  • Multiple Sclerosis Research Studies
  • CRISPR and Genetic Engineering
  • T-cell and Retrovirus Studies
  • Indigenous Health, Education, and Rights
  • Tuberculosis Research and Epidemiology
  • Primary Care and Health Outcomes
  • Diffusion and Search Dynamics
  • Herpesvirus Infections and Treatments

Banner Health
2024

Banner - University Medical Center Phoenix
2024

University of Birmingham
2009-2020

Immune Regulation (United Kingdom)
2012-2016

London School of Hygiene & Tropical Medicine
2016

Medical Research Council
2012

Cancer Research UK
2005-2009

Katherine Hospital
2005-2007

West Health
2005-2007

Harvard University
2006

The effects of a number mutations in the E.coli cyclic AMP receptor protein (CRP) have been determined by monitoring vivo expression and vitro open complex formation at two semi-synthetic promoters that are totally CRP-dependent. At one promoter CRP-blnding site is centred around 41.5 base pairs upstream from transcription start whilst other it 61.5 upstream. CRP mutation E171K reduces both H159L renders inactive: neither stops binding either promoter. K52N K52Q reverse effect ‘reeducate’ to...

10.1093/nar/18.24.7243 article EN Nucleic Acids Research 1990-01-01

Two factors contribute to Burkitt lymphoma (BL) pathogenesis, a chromosomal translocation leading c-myc oncogene deregulation and infection with Epstein-Barr virus (EBV). Although the has B cell growth-transforming ability, this may not relate its role in BL since many of transforming proteins are expressed tumor. Mounting evidence supports an alternative role, whereby EBV counteracts high apoptotic sensitivity inherent c-myc-driven growth program. In that regard, subset BLs carry mutants...

10.1371/journal.ppat.1000341 article EN cc-by PLoS Pathogens 2009-03-12

Epstein-Barr virus (EBV) infection often occurs in early childhood and is asymptomatic. However, if delayed until adolescence, primary may manifest as acute infectious mononucleosis (AIM), a febrile illness characterised by global CD8+ T-cell lymphocytosis, much of it reflecting huge expansion activated EBV-specific T-cells. While the events AIM have been intensely studied, little known about how these relate to asymptomatic infection. Here Gambian children (14–18 months old, an age at which...

10.1371/journal.ppat.1004746 article EN cc-by PLoS Pathogens 2015-03-27

ABSTRACT Epstein-Barr virus (EBV) is typically acquired asymptomatically in childhood. In contrast, infection later life often leads to infectious mononucleosis (IM), a febrile illness characterized by anti-EBV IgM antibody positivity, high loads of circulating latently infected B cells, and marked lymphocytosis caused hyperexpansion EBV-specific CD8 + T cells plus milder expansion CD56 dim NKG2A KIR − natural killer (NK) cells. How the two situations compare unclear due paucity studies on...

10.1128/jvi.00382-17 article EN cc-by Journal of Virology 2017-08-24

In Epstein-Barr virus (EBV)-transformed B lymphoblastoid and many Burkitt lymphoma cell lines, the EBV EBNA-1 protein is one of six viral nuclear antigens expressed from a common transcription unit under control two promoters, Wp or Cp. contrast, only antigen in other EBV-positive tumors. We previously identified promoter transcription, designated Fp, early-passage Mutu tumor cells, this also active long-term Akata lines which maintain exclusive expression characteristic tumor. However,...

10.1128/jvi.70.1.623-627.1996 article EN Journal of Virology 1996-01-01

Epstein–Barr virus (EBV), a human herpesvirus, transforms B cell growth in vitro through expressing six virus-coded nuclear antigens (EBNAs) and two latent membrane proteins (LMPs). In many EBV-associated tumors, however, viral antigen expression is more restricted, the aetiological role of unclear. For example, endemic Burkitt lymphoma (BL) classically presents as monoclonal, c-myc-translocation-positive tumor which every carries EBV an EBNA1-only (Latency I) infection; such homogeneity...

10.1073/pnas.0509988103 article EN Proceedings of the National Academy of Sciences 2006-09-26

The Epstein-Barr virus (EBV)-encoded leader protein EBNA-LP is made up of several 66-amino-acid repeats (the W1W2 domains) linked to a unique 45-amino-acid C-terminal sequence Y1Y2 domain). This highly expressed along with second nuclear antigen, EBNA-2, during the initial stages virus-induced B-cell transformation. While EBNA-2's essential role in transformation as transcriptional activatory well documented, very little known about function except that recombinant viruses lacking exons show...

10.1128/jvi.71.9.6619-6628.1997 article EN Journal of Virology 1997-09-01

Studies of Epstein-Barr virus (EBV)-positive cell lines have identified several forms latency, but the patterns gene expression in EBV-positive tumour cells appear more variable. However, it is unclear to what extent these differences merely reflect increased sensitivities different detection methods. Here, design and validation novel real-time RT-PCR assays quantify relative levels EBV transcripts are described. When new were used screen a collection endemic Burkitt's lymphoma tumours,...

10.1099/vir.0.81906-0 article EN Journal of General Virology 2006-09-08

Epstein-Barr virus (EBV) is associated with malignant diseases of lymphoid and epithelial cell origin. The tropism EBV due to B-cell-restricted expression CD21, the major receptor molecule for virus. However, efficient infection CD21- cells can be achieved via transfer from EBV-coated B cells. We compare contrast here early events following in vitro primary Using sensitive, quantitative reverse transcription-PCR assays several latent lytic transcripts two-color immunofluorescence staining...

10.1128/jvi.00108-09 article EN Journal of Virology 2009-05-14

ABSTRACT Epstein-Barr virus (EBV) has been shown to encode at least 40 microRNAs (miRNAs), an important class of molecules that negatively regulate the expression many genes through posttranscriptional mechanisms. Here, we have used real-time PCR assays quantify levels EBV-encoded BHRF1 and BART miRNAs in latently infected cells induced into lytic cycle. During latency, were seen only with detectable Cp- and/or Wp-initiated EBNA transcripts, while expressed all forms latent infection....

10.1128/jvi.01528-10 article EN Journal of Virology 2010-11-11

To investigate how intense Plasmodium falciparum infection predisposes to Epstein-Barr virus (EBV)-positive Burkitt lymphoma (BL), we analyzed the effect of acute malaria on existing EBV-host balance.EBV genome loads in peripheral blood mononuclear cells were assayed by quantitative polymerase chain reaction, and EBV-specific CD8(+) T cell responses interferon-gamma enzyme-linked immunospot assay.Gambian children, from whom samples obtained during an attack again up 6 weeks later, had...

10.1086/594373 article EN The Journal of Infectious Diseases 2008-11-25

Disruption of T cell memory during severe immune suppression results in reactivation chronic viral infections, such as Epstein Barr virus (EBV) and Cytomegalovirus (CMV). How different subsets cells contribute to the protective immunity against these viruses remains poorly defined. In this study we examined compartmentalization virus-specific, tissue resident CD8+ human lymphoid organs. This revealed two distinct populations cells, that were CD69+CD103+ CD69+CD103-, retained within spleen...

10.1371/journal.ppat.1005799 article EN cc-by PLoS Pathogens 2016-08-19

We have validated a flexible, high-throughput and relatively inexpensive RT-QPCR array platform for absolute quantification of Epstein–Barr virus transcripts in different latent lytic infection states. Several novel observations are reported. First, during normal B cells, Wp-initiated gene remain far more abundant following activation the Cp promoter than was hitherto suspected. Second, EBNA1 transcript levels remarkably low all forms latency, typically ranging from 1 to 10 per cell. EBNA3A,...

10.1016/j.virol.2014.10.030 article EN cc-by Virology 2014-11-15

Most Epstein-Barr virus (EBV)-positive Burkitt's lymphomas (BLs) carry a wild-type EBV genome and express nuclear antigen 1 (EBNA1) selectively from the BamHI Q promoter (latency I). Recently we identified distinct subset of BLs carrying both EBNA2 gene-deleted (transformation-defective) viral genomes. The cells displayed an atypical "BamHI W (Wp)-restricted" form latency where Wp (rather than Qp) was active EBNA1, -3A, -3B, -3C, -LP were expressed in absence or latent membrane proteins 2....

10.1128/jvi.79.16.10709-10717.2005 article EN Journal of Virology 2005-07-28

Expression from the E.coli melR promoter (pmelR) is normally totally dependent on transcription activator protein, CRP. We describe experiments with a genetically engineered DNA fragment carrying pmelR in which wild type CRP binding site was replaced synthetic oligonucleotides containing either FNR or sequences. When oligonucleotide contains 22 bp consensus for sites, expression but not Single changes at of two symmetrically-related positions create sites that are recognised by both and...

10.1093/nar/17.10.3865 article EN Nucleic Acids Research 1989-01-01

The gamma-herpesvirus Epstein-Barr virus (EBV) persists for life in infected individuals despite the presence of a strong immune response. During lytic cycle EBV many viral proteins are expressed, potentially allowing virally cells to be recognized and eliminated by CD8+ T cells. We have recently identified an evasion protein encoded EBV, BNLF2a, which is expressed early phase replication inhibits peptide- ATP-binding functions transporter associated with antigen processing. Ectopic...

10.1371/journal.ppat.1000490 article EN cc-by PLoS Pathogens 2009-06-25
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