Epstein-barr virus immortalization and latency

Rowe, David

doi:10.2741/a433

Cited by 33 publications

(40 citation statements)

References 44 publications

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“…Although lifetime immunity to EBV is apparently achieved in normal individuals, this virus is not completely eradicated and persists in a latent infection state (3)(4)(5), which is effectively controlled by the EBV-specific T lymphocytes (2). However, in immunosuppressed individuals such as transplant patients, primary EBV infection usually results in posttransplant lymphoproliferative disorders (PTLD) that often progress into B cell lymphomas (6 -8).…”

Section: Inhibition Of Ebv-induced Lymphoproliferation By Cd4mentioning

confidence: 99%

Inhibition of EBV-Induced Lymphoproliferation by CD4+ T Cells Specific for an MHC Class II Promiscuous Epitope

Omiya¹,

Buteau

Kobayashi³

et al. 2002

The Journal of Immunology

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Posttransplant lymphoproliferative disorder (PTLD) and B cell lymphomas induced by EBV continue to be a major life-threatening complication in transplant patients. The establishment and enhancement of T cell immunity to EBV before transplantation and immunosuppressive therapy could help diminish these complications, but the lack of an effective vaccine has limited this prophylactic approach. We describe here the identification of a peptide epitope from the EBV EBNA2 Ag that is capable of inducing in vitro CD4+ T cell responses that inhibit the EBV-mediated B lymphocyte proliferation associated with PTLD. Most significantly, T cell responses to the EBNA2 epitope were found to be restricted by numerous MHC class II alleles (DR1, DR7, DR16, DR52, DQ2, and DQ7), indicating that this peptide is highly promiscuous and would be recognized by a large proportion (>50%) of the general population. These results are relevant for the design of a simple, inexpensive and widely applicable peptide-based vaccine to prevent PTLD in solid organ transplant patients.

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Section: Inhibition Of Ebv-induced Lymphoproliferation By Cd4mentioning

confidence: 99%

Inhibition of EBV-Induced Lymphoproliferation by CD4+ T Cells Specific for an MHC Class II Promiscuous Epitope

Omiya¹,

Buteau

Kobayashi³

et al. 2002

The Journal of Immunology

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“…It is proposed that viral latency is either a separate (parallel pathway model) or downstream consequence (serial pathway model) of immortalization events [78]. Studies on LMP2 and its involvement in various signaling pathways provide important clues on viral latency and malignant transformation.…”

Section: The Signaling Pathway Of Lmp2a In Viral Latency and Cancermentioning

confidence: 99%

The signaling pathways of Epstein-Barr virus-encoded latent membrane protein 2A (LMP2A) in latency and cancer

Pang

Lin

Peh

2009

Cellular and Molecular Biology Letters

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Epstein-Barr virus (EBV) is a ubiquitous virus with infections commonly resulting in a latency carrier state. Although the exact role of EBV in cancer pathogenesis remains not entirely clear, it is highly probable that it causes several lymphoid and epithelial malignancies, such as Hodgkin's lymphoma, NK-T cell lymphoma, Burkitt's lymphoma, and nasopharyngeal carcinoma. EBV-associated malignancies are associated with a latent form of infection, and several of these EBV-encoded latent proteins are known to mediate cellular transformation. These include six nuclear antigens and three latent membrane proteins. Studies have shown that EBV displays distinct patterns of viral latent gene expression in these lymphoid and epithelial tumors. The constant expression of latent membrane protein 2A (LMP2A) at the RNA level in both primary and metastatic tumors suggests that this protein might be a driving factor in the tumorigenesis of EBV-associated malignancies. LMP2A may cooperate with the aberrant host genome, and thereby contribute to malignant transformation by intervening in signaling pathways at multiple points, especially in the cell cycle and apoptotic pathway. This review summarizes the role of EBV-encoded LMP2A in EBV-associated viral latency and cancers. We will focus our discussions on the molecular interactions of each of the conserved motifs in LMP2A, and their involvement in various signaling pathways, namely the B-cell receptor blockade mechanism, the ubiquitin-mediated (Notch and Wnt) pathways, and the MAPK, PI3-K/Akt, NK-κB and STAT pathways, which can provide us with important insights into the roles of LMP2A in the EBVassociated latency state and various malignancies.

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“…EBV can establish three types of latency, I, II and III (Kerr et al, 1992;Rowe, 1999) associated with malignancy, characterized by the differential expression of the latency proteins. One of these proteins, EBV nuclear antigen 1 (EBNA1) is expressed during all three types of latent infection and is the only protein absolutely required to maintain latency (Marechal et al, 1999;Kieff and Rickinson 2001).…”

Section: Introductionmentioning

confidence: 99%

Epstein–Barr virus U leader exon contains an internal ribosome entry site

2003

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Eukaryotic translation can be initiated either by a capdependent mechanism or by internal ribosome entry, a process by which ribosomes are directly recruited to structured regions of mRNA upstream of the initiation codon. Here we report the finding of an internal ribosome entry site (IRES) in the untranslated region of the Epstein-Barr nuclear antigen 1 (EBNA1) gene. EBNA1 is the only nuclear protein expressed in all known states of Epstein-Barr virus (EBV) latency and in the virus lytic cycle, and is required for the maintenance of the EBV episome. Using cDNA reporter constructs and in vitro transfection assays, we found that sequences contained in the 5 0 untranslated region (UTR) of the Fp and Qp initiated EBNA1 mRNA increased the expression level 4-14-fold in different Burkitt lymphoma cell lines. The U leader exon, located within the 5 0 UTR, included in all known EBNA1 transcripts and also contained in the EBNA3, 4 and 6 mRNAs, was demonstrated by bicistronic expression analyses to contain an IRES. The EBNA IRES initiates translation more efficiently than the encephalomyocarditis virus IRES in EBV-positive lymphoma cells. We propose that the EBNA IRES constitute a novel mechanism, whereby EBV regulates latent gene expression.

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Epstein-barr virus immortalization and latency

Cited by 33 publications

References 44 publications

Inhibition of EBV-Induced Lymphoproliferation by CD4+ T Cells Specific for an MHC Class II Promiscuous Epitope

Inhibition of EBV-Induced Lymphoproliferation by CD4+ T Cells Specific for an MHC Class II Promiscuous Epitope

The signaling pathways of Epstein-Barr virus-encoded latent membrane protein 2A (LMP2A) in latency and cancer

Epstein–Barr virus U leader exon contains an internal ribosome entry site

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