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Epstein–Barr virus: 40 years on
by
Young, Lawrence S.
, Rickinson, Alan B.
in
Antigens, Viral - genetics
/ Antigens, Viral - physiology
/ B-Lymphocytes - pathology
/ B-Lymphocytes - virology
/ Biomedical and Life Sciences
/ Biomedicine
/ Burkitt Lymphoma - epidemiology
/ Burkitt Lymphoma - virology
/ Cancer Research
/ Carcinoma - therapy
/ Carcinoma - virology
/ Cell Transformation, Neoplastic
/ Cell Transformation, Viral
/ Epstein-Barr virus
/ Epstein-Barr Virus Infections - pathology
/ Epstein-Barr Virus Infections - virology
/ Herpesvirus 4, Human - genetics
/ Herpesvirus 4, Human - pathogenicity
/ Herpesvirus 4, Human - physiology
/ Humans
/ Immunocompromised Host
/ Killer Cells, Natural - pathology
/ Lymphoma - therapy
/ Lymphoma - virology
/ Lymphoma, B-Cell - immunology
/ Lymphoma, B-Cell - virology
/ Lymphoma, T-Cell - virology
/ Nasopharyngeal Neoplasms - epidemiology
/ Nasopharyngeal Neoplasms - virology
/ review-article
/ Stomach Neoplasms - virology
/ Viral Proteins - genetics
/ Viral Proteins - physiology
/ Virus Latency
2004
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Epstein–Barr virus: 40 years on
by
Young, Lawrence S.
, Rickinson, Alan B.
in
Antigens, Viral - genetics
/ Antigens, Viral - physiology
/ B-Lymphocytes - pathology
/ B-Lymphocytes - virology
/ Biomedical and Life Sciences
/ Biomedicine
/ Burkitt Lymphoma - epidemiology
/ Burkitt Lymphoma - virology
/ Cancer Research
/ Carcinoma - therapy
/ Carcinoma - virology
/ Cell Transformation, Neoplastic
/ Cell Transformation, Viral
/ Epstein-Barr virus
/ Epstein-Barr Virus Infections - pathology
/ Epstein-Barr Virus Infections - virology
/ Herpesvirus 4, Human - genetics
/ Herpesvirus 4, Human - pathogenicity
/ Herpesvirus 4, Human - physiology
/ Humans
/ Immunocompromised Host
/ Killer Cells, Natural - pathology
/ Lymphoma - therapy
/ Lymphoma - virology
/ Lymphoma, B-Cell - immunology
/ Lymphoma, B-Cell - virology
/ Lymphoma, T-Cell - virology
/ Nasopharyngeal Neoplasms - epidemiology
/ Nasopharyngeal Neoplasms - virology
/ review-article
/ Stomach Neoplasms - virology
/ Viral Proteins - genetics
/ Viral Proteins - physiology
/ Virus Latency
2004
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Epstein–Barr virus: 40 years on
by
Young, Lawrence S.
, Rickinson, Alan B.
in
Antigens, Viral - genetics
/ Antigens, Viral - physiology
/ B-Lymphocytes - pathology
/ B-Lymphocytes - virology
/ Biomedical and Life Sciences
/ Biomedicine
/ Burkitt Lymphoma - epidemiology
/ Burkitt Lymphoma - virology
/ Cancer Research
/ Carcinoma - therapy
/ Carcinoma - virology
/ Cell Transformation, Neoplastic
/ Cell Transformation, Viral
/ Epstein-Barr virus
/ Epstein-Barr Virus Infections - pathology
/ Epstein-Barr Virus Infections - virology
/ Herpesvirus 4, Human - genetics
/ Herpesvirus 4, Human - pathogenicity
/ Herpesvirus 4, Human - physiology
/ Humans
/ Immunocompromised Host
/ Killer Cells, Natural - pathology
/ Lymphoma - therapy
/ Lymphoma - virology
/ Lymphoma, B-Cell - immunology
/ Lymphoma, B-Cell - virology
/ Lymphoma, T-Cell - virology
/ Nasopharyngeal Neoplasms - epidemiology
/ Nasopharyngeal Neoplasms - virology
/ review-article
/ Stomach Neoplasms - virology
/ Viral Proteins - genetics
/ Viral Proteins - physiology
/ Virus Latency
2004
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Journal Article
Epstein–Barr virus: 40 years on
2004
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Overview
Key Points
Epstein–Barr virus (EBV) infection is implicated in the aetiology of several different lymphoid and epithelial malignancies.
EBV-encoded latent genes induce B-cell transformation
in vitro
by altering cellular gene transcription and constitutively activating key cell-signalling pathways.
EBV exploits the physiology of normal B-cell differentiation to persist within the memory-B-cell pool of the immunocompetent host.
Immunosuppressed transplant patients are at risk of developing fatal EBV-transformed B-cell proliferations, presenting as 'post-transplant lymphomas'.
Other EBV-associated tumours show more restricted forms of latent gene expression, reflecting a more complex pathogenesis that involves additional cofactors.
Pharmacological and immunotherapeutic approaches are being developed to treat or prevent EBV-associated tumours.
Epstein–Barr virus (EBV) was discovered 40 years ago from examining electron micrographs of cells cultured from Burkitt's lymphoma, a childhood tumour that is common in sub-Saharan Africa, where its unusual geographical distribution — which matches that of holoendemic malaria —indicated a viral aetiology. However, far from showing a restricted distribution, EBV — a γ-herpesvirus — was found to be widespread in all human populations and to persist in the vast majority of individuals as a lifelong, asymptomatic infection of the B-lymphocyte pool. Despite such ubiquity, the link between EBV and 'endemic' Burkitt's lymphoma proved consistent and became the first of an unexpectedly wide range of associations discovered between this virus and tumours.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Antigens, Viral - physiology
/ Biomedical and Life Sciences
/ Burkitt Lymphoma - epidemiology
/ Cell Transformation, Neoplastic
/ Epstein-Barr Virus Infections - pathology
/ Epstein-Barr Virus Infections - virology
/ Herpesvirus 4, Human - genetics
/ Herpesvirus 4, Human - pathogenicity
/ Herpesvirus 4, Human - physiology
/ Humans
/ Killer Cells, Natural - pathology
/ Lymphoma, B-Cell - immunology
/ Nasopharyngeal Neoplasms - epidemiology
/ Nasopharyngeal Neoplasms - virology
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