The role of Epstein–Barr virus in cancer

  title={The role of Epstein–Barr virus in cancer},
  author={Samuel B. Pattle and Paul J. Farrell},
  journal={Expert Opinion on Biological Therapy},
  pages={1193 - 1205}
  • S. Pattle, P. Farrell
  • Published 18 October 2006
  • Biology, Medicine
  • Expert Opinion on Biological Therapy
Epstein–Barr virus (EBV), discovered > 40 years ago from a Burkitt’s lymphoma biopsy, was the first virus to be directly associated with human cancer. EBV has two distinct life cycles in the human host; a lytic form of infection that produces new infectious virions, and a latent form of infection that allows the virus to persist in a dormant state for the lifetime of the host. EBV has evolved a life cycle that mimics the natural differentiation pathway of antigen-activated B cells, giving the… 

A Review of the Cytomorphology of Epstein-Barr Virus-Associated Malignancies

The unique cytomorphology and ancillary studies required to diagnose EBV-related neoplasms are discussed, including HIV-infection or transplant-related immunosuppression, which are often all required to make a diagnosis ofEBV-associated malignancy.

Epstein-Barr Virus – pathogenesis, latency andcancers

EBV frequency and its association with the occurrence of malignant tumours and the pathways of tumour progression are discussed.

Detection of Epstein-Barr virus in T-cell prolymphocytic leukemia cells in vitro.

  • K. LanM. Murakami E. Robertson
  • Biology, Medicine
    Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
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In response to the immune system of the body, EBV miRNAs can inhibit the expression and presentation of viral antigens, inhibit immune activation and immunotoxicity, assisting host cells to escape from immunity, and providing conditions for further immortalized tumorigenesis of the host cells.

Epstein-Barr Virus Type 2 Infects T Cells and Induces B Cell Lymphomagenesis in Humanized Mice

An EBV-2 humanized mouse model is developed, utilizing immunodeficient mice engrafted with human cord blood CD34+ stem cells, that establishes a latency III infection with evidence of ongoing viral reactivation in both B and T cells and efficiently induces lymphomagenesis in humanized mice.

Epstein Barr Virus genome variation and functional analysis of the IR-1 internal repeat

Through the production of an inverted repeat knockout B95-8 EBV BAC, this study found that the inverted repeat is essential for B cell immortalisation and plays a role in virus production.

An oncogenic Epstein Barr virus developing diseases and cancer in human

The present paper deals with the study of Epstein Barr virus causing several diseases including cancer in human, which ranges from infectious mononucleosis to the cancerous Burkitt’s lymphoma.



Activation of Epstein–Barr virus latent genes protects human B cells from death by apoptosis

It is shown in an in vitro system that EBV, through expression of the full set of eight virus-coded 'latent' proteins, can protect human B cells from programmed cell death (apoptosis), the deletion mechanism which normally restricts entry into memory.

Demonstration of the Burkitt's lymphoma Epstein-Barr virus phenotype in dividing latently infected memory cells in vivo

It is shown that most infected cells in the blood express no detectable latent mRNA or proteins, which suggests that BL may be a tumor of a latently infected memory B cell that is stuck proliferating because it is a tumor and, therefore, constitutively expressing only EBNA1.

Epstein-Barr virus provides a survival factor to Burkitt's lymphomas

It is demonstrated that one viral protein found in allEBV-associated malignancies, Epstein-Barr nuclear antigen 1 (EBNA-1), is required for survival of one of these cancers, EBV-positive Burkitt's lymphoma, and by extension, for the other B cell tumors with which EBV is associated.

Epstein–Barr virus–associated Burkitt lymphomagenesis selects for downregulation of the nuclear antigen EBNA2

A subset of BL tumors in which the Latency III-associated EBNA promoter Wp is active and most EBNAs are expressed, but where a gene deletion has specifically abrogated the expression of EBNA2 is identified, implying that BL can be selected from a Latencies III progenitor and that the principal selection pressure is for downregulation of the c-Myc antagonist EBNA 2.

Immunohistology of Epstein-Barr virus-associated antigens in B cell disorders from immunocompromised individuals.

Proliferating B cell lesions developing in a series of immunosuppressed organ transplant recipients and patients with X-linked lymphoproliferative syndrome were examined for Epstein-Barr virus and cellular gene expression using immunocytochemistry and immunoblotting techniques, and results indicate that all the lesions examined were consistent with a latent, nonproductive type of infection.

Circulating Epstein-Barr virus-carrying B cells in acute malaria

Tonsillar memory B cells, latently infected with Epstein-Barr virus, express the restricted pattern of latent genes previously found only in Epstein-Barr virus-associated tumors.

It is suggested that the transcription pattern found in latently infected, tonsillar, memory B cells is used because it allows for the expression of LMP1, LMP2a, and EBNA1 in the absence of the immunogenic and growth-promoting EBNA2 andEBNA3 molecules.

Epstein–Barr virus: 40 years on

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.