Transformation of lymphocytes by herpesvirus papio

Falk, Lawrence A.; Henle, Gertrude; Henle, Werner; Deinhardt, Friedrich; A, Schudel

doi:10.1002/ijc.2910200209

Cited by 38 publications

(12 citation statements)

References 19 publications

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“…Several lines of evidence suggesting association of this virus with baboon malignant lymphoma were found which paralleled those known for association of EBV and Burkitt's lymphoma. (Rabin et al, 1977;Falk et al, 1977;Deinhardt et al, 1978;Djatchenko et al, 1980). On the other hand in the most representative and thoroughly controlled seroepizootiological study no significant difference was found between anti-HVP titers from the lymphomatous and the healthy baboon groups (Lapin et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Increased antibody responses to Herpes virus papio (HVP) ANTIGENS IN PRE‐LYMPHOMATOUS BABOONS (Papio hamadryas) of the sukhumi high lymphoma stock

Voevodin¹,

Yakovleva²,

Лапин³

et al. 1983

Intl Journal of Cancer

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Antibody responses to Herpes virus papio (HVP) antigens were studied in 21 pre-lymphoma baboons (which subsequently died of malignant lymphoma), 21 paired controls, i.e. age-, sex- and population-matched healthy baboons, and 185 randomly selected healthy baboons of the same population. The sera were all collected at the same time and were tested blind in the fixed-cell indirect immunofluorescence test against HVP viral capsid antigen (VCA)-positive, early antigen (EA)-positive cell targets before and after absorption with HVP. Eleven of the pre-lymphoma sera were anti-EA-positive whereas none of the paired controls contained anti-EA. Anti-VCA titers of pre-lymphoma sera were higher than those of paired controls in thirteen cases. Only in four cases were anti-VCA titers of pre-lymphoma sera lower than those of paired controls. Qualitatively, the same results were obtained when anti-VCA and anti-EA titers of pre-lymphoma sera were compared with respective mean population values. The differences between pre-lymphoma group and control groups, especially in the case of anti-EA, were statistically highly significant. Thus, elevated anti-HVP titers in healthy baboons of the Sukhumi lymphoma-prone stock can be considered as a marker of high risk for development of malignant lymphoma.

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Section: Discussionmentioning

confidence: 99%

Increased antibody responses to Herpes virus papio (HVP) ANTIGENS IN PRE‐LYMPHOMATOUS BABOONS (Papio hamadryas) of the sukhumi high lymphoma stock

Voevodin¹,

Yakovleva²,

Лапин³

et al. 1983

Intl Journal of Cancer

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“…Importantly, many of the defining properties of EBV are conserved in these related LCVs, including immortalization of host B lymphocytes in vitro, establishment of lifelong infection, and induction of diseases similar to those commonly associated with EBV, namely, infectious mononucleosis, lymphoproliferative disease, and lymphomas (8,9,13,37,38). Not surprisingly, the genomes of EBV and the nonhuman primate LCVs characterized to date are colinear and highly homologous with some ORFs displaying striking homology to their EBV counterparts, e.g., the latency-associated proteins EBNA-1 and EBNA-LP and the lytic cycle protein BHRF-1 (56, 61 and 64% amino acid identity, respectively) (18-20, 40, 56).…”

mentioning

confidence: 99%

Transcriptional Regulatory Properties of Epstein-Barr Virus Nuclear Antigen 3C Are Conserved in Simian Lymphocryptoviruses

Dalbiès-Tran

Jiang

Ruf

et al. 2003

J Virol

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Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA-3C) is a large transcriptional regulator essential for EBV-mediated immortalization of B lymphocytes. We previously identified interactions between EBNA-3C and two cellular transcription factors, J and Spi proteins, through which EBNA-3C regulates transcription. To better understand the contribution of these interactions to EBNA-3C function and EBV latency, we examined whether they are conserved in the homologous proteins of nonhuman primate lymphocryptoviruses (LCVs), which bear a strong genetic and biological similarity to EBV. The homologue of EBNA-3C encoded by the LCV that infects baboons (BaLCV) was found to be only 35% identical in sequence to its EBV counterpart. Of particular significance, this homology localized predominantly to the N-terminal half of the molecule, which encompasses the domains in EBNA-3C that interact with J and Spi proteins. Like EBNA-3C, both BaLCV and rhesus macaque LCV (RhLCV) 3C proteins bound to J and repressed transcription mediated by EBNA-2 through its interaction with J. Both nonhuman primate 3C proteins were also able to activate transcription mediated by the Spi proteins in the presence of EBNA-2. Like EBNA-3C, a domain encompassing the putative basic leucine zipper motif of the BaLCV-3C protein directly interacted with both Spi-1 and Spi-B. Surprisingly, a recently identified motif in EBNA-3C that mediates repression was not identifiable in the BaLCV-3C protein.Finally, although the C terminus of BaLCV-3C bears minimal homology to EBNA-3C, it nonetheless contains a C-terminal domain rich in glutamine and proline that was able to function as a potent transcriptional activation domain, as does the C terminus of EBNA-3C. The conservation of these functional motifs despite poor overall homology among the LCV 3C proteins strongly suggests that the interactions of EBNA-3C with J and Spi do indeed play significant roles in the life cycle of EBV.Studies using recombinant Epstein-Barr virus (EBV) genomes have identified six latent infection proteins that are essential for EBV-mediated immortalization of B lymphocytes in vitro: EBV nuclear antigen 1 (EBNA-1), EBNA-2, EBNA-LP, EBNA-3A, EBNA-3C, and latent membrane protein (LMP) 1 (5,17,27,29,34,53). Two of these viral proteins, and perhaps the least well understood, are members of the EBNA-3 family of transcriptional regulators. Although the three EBNA-3 genes (3A, 3B, and 3C) share a similar gene structure and are likely to have evolved from a common ancestral gene, the encoded proteins are highly divergent in amino acid sequence. The EBNA-3 proteins are also likely to have diverged functionally, since EBNA-3A and EBNA-3C, but not EBNA-3B, are essential for EBV-mediated immortalization of B lymphocytes. Despite their differences, all EBNA-3 proteins function as transcriptional regulatory proteins whose transcriptional effects are mediated through interactions with cellular sequence-specific DNA-binding proteins, rather than by binding directly to DNA (26,45,50,57,58). In addition to...

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“…This is understandable, because they carry EBV-related herpesviruses that induce cross-neutralizing antibodies. The EBV-like chimpanzee, baboon, and orangoutan viruses were studied in some detail (26)(27)(28)(29) (33). 14q+ markers were subsequently described in a variety of other lymphoreticular neoplasias (31,(34)(35)(36)(37)(38)(39) We have previously suggested (42) that BL develops in at least three steps.…”

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confidence: 99%

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Klein¹

1979

Proc. Natl. Acad. Sci. U.S.A.

261

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Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell Iymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.

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Transformation of lymphocytes by herpesvirus papio

Cited by 38 publications

References 19 publications

Increased antibody responses to Herpes virus papio (HVP) ANTIGENS IN PRE‐LYMPHOMATOUS BABOONS (Papio hamadryas) of the sukhumi high lymphoma stock

Increased antibody responses to Herpes virus papio (HVP) ANTIGENS IN PRE‐LYMPHOMATOUS BABOONS (Papio hamadryas) of the sukhumi high lymphoma stock

Transcriptional Regulatory Properties of Epstein-Barr Virus Nuclear Antigen 3C Are Conserved in Simian Lymphocryptoviruses

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

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