Restricted expression of EBV latent genes and T-lymphocyte-detected membrane antigen in Burkitt's lymphoma cells.

Rowe, David; Rowe, Martin; Evan, Gérard I.; Wallace, L. E.; Farrell, Patrick J.; Rickinson, Alan B.

doi:10.1002/j.1460-2075.1986.tb04540.x

Cited by 191 publications

(110 citation statements)

References 42 publications

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“…However, the existence of discrete latency programs is strongly supported by studies of EBV-associated malignancies (Table 1). Thus, Latency III is expressed in the immunoblast-like cells of EBV carrying lymphoproliferative disorders arising in organ and bone marrow transplant recipients and HIV patients (Thomas et al, 1991), while Latency I is found in EBV carrying Burkitt's lymphomas (BLs) that are phenotypically similar to memory B lymphocytes (Rowe et al, 1986). In line with the germinal center origin of Hodgkin's disease (HD) lymphomas, cells from EBV-positive HD express a Latency II program (reviewed in Niedobitek et al, 2000).…”

Section: Ebv Latency and Oncogenesismentioning

confidence: 99%

“…A genetically and phenotypically similar but EBV-negative variant of the tumor is found all over the world suggesting that EBV infection acts as a cofactor in the pathogenesis of this malignancy. Only EBNA-1 is usually detected in the EBV positive tumors (Rowe et al, 1986), although tumors expressing EBNA-1 together with the high molecular weight EBNA-3, -4 and -6 were recently described (Kelly et al, 2002). In all cases, the viral EBNA-2 and LMP-1 are not expressed and, as a result, EBV-positive BL cells do not express B-cell activation markers, adhesion and costimulatory molecules and grow as single cell suspensions rather than in clumps (Rowe et al, 1986).…”

Section: The Rescue Program: Lmp-2a and The Capture Of Cellular Ubiqumentioning

confidence: 99%

“…Only EBNA-1 is usually detected in the EBV positive tumors (Rowe et al, 1986), although tumors expressing EBNA-1 together with the high molecular weight EBNA-3, -4 and -6 were recently described (Kelly et al, 2002). In all cases, the viral EBNA-2 and LMP-1 are not expressed and, as a result, EBV-positive BL cells do not express B-cell activation markers, adhesion and costimulatory molecules and grow as single cell suspensions rather than in clumps (Rowe et al, 1986). Characteristic for the tumor cells are also the low levels of MHC class I and selective loss of certain class I alleles, HLA A11 in particular (Andersson et al, 1991), which may contribute to the poor allostimulatory capacity of these cells in mixed lymphocyte cultures (Avila-Carino et al, 1987).…”

Section: The Rescue Program: Lmp-2a and The Capture Of Cellular Ubiqumentioning

confidence: 99%

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Epstein–Barr virus oncogenesis and the ubiquitin–proteasome system

Masucci

2004

Oncogene

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Epstein-Barr virus (EBV), a human herpesvirus associated with lymphoid and epithelial cell tumors, encodes several proteins that exploit the ubiquitin-proteasome system to regulate latency and allow the persistence of infected cells in immunocompetent hosts. Further modifications of ubiquitin-dependent proteolysis by activated cellular oncogenes contribute to malignant transformation. A detailed understanding of these processes may lead to the development of new therapeutic strategies for EBVassociated cancers.

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Section: Ebv Latency and Oncogenesismentioning

confidence: 99%

Section: The Rescue Program: Lmp-2a and The Capture Of Cellular Ubiqumentioning

confidence: 99%

Section: The Rescue Program: Lmp-2a and The Capture Of Cellular Ubiqumentioning

confidence: 99%

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Epstein–Barr virus oncogenesis and the ubiquitin–proteasome system

Masucci

2004

Oncogene

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“…In type I latency, only the EBNA1 protein is expressed (64). It has recently been shown that EBNA1 peptides do not enter the major histocompatibility complex class I antigen processing and presentation pathway (29,39,52), and cells which express only EBNA1 are not detected by host cellular immune surveillance mechanisms (63).…”

Section: Epstein-barr Virus (Ebv) Infection In Immunocompetentmentioning

confidence: 99%

Constitutive Activation of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Gene Transcription by IRF1 and IRF2 during Restricted EBV Latency

Schaefer

Paulson

Strominger

et al. 1997

Molecular and Cellular Biology

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Epstein-Barr virus (EBV) infection in immunocompetenthumans is predominantly latent and persists for the life of the individual (reviewed in reference 41). Recently, it has been shown that EBV is capable of adopting at least three distinct forms of latency (27). Type III latency is observed upon in vitro infection of B lymphocytes and results in immortalization and continuous proliferation of the infected B cells via the action of a subset of the six EBV nuclear antigens (EBNAs; EBNA1, EBNA2, EBNA3a, EBNA3b, EBNA3c, and EBNA4) and three membrane proteins (LMP1, LMP2a, and LMP2b) expressed in the type III (immortalizing) program. However, in vivo, the type III latency program is likely to be only transiently observed upon initial infection of a naive host, since several of the type III latent antigens elicit a potent cytotoxic T-lymphocyte response resulting in very effective elimination of type III latently infected B cells (reviewed in reference 33).EBV is also capable of entering programs of latency in which the expression of latent antigens is restricted with respect to the type III program. In type I latency, only the EBNA1 protein is expressed (64). It has recently been shown that EBNA1 peptides do not enter the major histocompatibility complex class I antigen processing and presentation pathway (29, 39, 52), and cells which express only EBNA1 are not detected by host cellular immune surveillance mechanisms (63). The type II latency program differs from type I latency only in the expression of variable combinations of LMP1, LMP2a, and LMP2b, in addition to EBNA1. Since the type I latency program was identified, there has been speculation that type I latently infected B lymphocytes represent the lifelong reservoir of virus in immunocompetent, seropositive individuals, and there have recently been several reports which provide evidence that a type I-like form of restricted viral latency does indeed exist in healthy carriers of EBV (6,51,60,85).Investigations into the molecular basis of type III and type I latency have demonstrated that distinct promoters are used to drive transcription of the EBNAs in each latent program. In type III latency, transcription of all six nuclear antigens is initiated from either Wp (during initial infection of resting B cells) or Cp (in cycling B cells), and the long primary transcripts are differentially spliced to generate the mature EBNA transcripts (75, 94; see Fig. 1A for a schematic representation of EBV latent transcription and locations of promoters). Recent investigations have shown that transcription of the EBNA1 gene in type I latency is driven by a promoter designated Qp, which is considerably downstream of the type III latency EBNA gene promoters (57,(70)(71)(72). Qp has an architecture with numerous similarities to eukaryotic housekeeping

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“…6 Upon prolonged cultivation in vitro the cells start to express the whole set of viral genes expressed in EBV immortalized lymphocytes (Group III) and as a consequence, start to express a variety of adhesion molecules and activation markers. 6,7 We have been interested to better understand to which degree EBV and the c-myc oncogene contribute to the phenotype and growth pattern of BL cells. To this end, we have attempted to reconstruct some of the essential features of BL cells in vitro starting from primary normal human B lymphocytes.…”

mentioning

confidence: 99%