Mechanisms of Viral Tumorigenesis

Gilden, Raymond V.; Rabin, Harvey

doi:10.1016/s0065-3527(08)60437-6

Cited by 8 publications

(5 citation statements)

References 214 publications

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“…As such, it is a member of a large group of primate lymphotropic herpesviruses, which includes the B-cell tropic Epstein-Barr virus (EBV) of man, the EBV-like viruses of Old World monkeys and apes, and the T-cell tropic viruses of New World monkeys (1). HVS is not pathogenic for squirrel monkeys but is potently oncogenic for several other species of New World monkeys and rabbits, where it produces fatal T-cell lymphomas and leukemias (2)(3)(4)(5)(6)(7)(8). Although HVS readily produces T-cell lymphomas in New World primates, only one lymphoid cell line has been established by in vitro transformation (9).…”

mentioning

confidence: 99%

Transformation of owl monkey T cells in vitro with Herpesvirus saimiri.

Rabin¹,

Hopkins²,

Desrosiers³

et al. 1984

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

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Owl monkey peripheral blood mononuclear cells were treated with phytohemagglutinin and expanded in interleukin 2 (IL-2)-containing medium. The cells were then exposed to Herpesvirus saimiri (HVS strain S295C)-infected owl monkey kidney monolayer cells. Four to 6 weeks later, the lymphocytes showed increased clumping and cell growth and the ability to grow in the absence of IL-2. Control lymphocyte cultures not exposed to HVS eventually died out at '=6-8 weeks, even in the presence of IL-2. Although infected lymphocytes grew 'continuously in the absence of IL-2, their growth was enhanced by addition of IL-2 to the cultures. Natural killer cell-like cytotoxicity and -interferon release were also enhanced by IL-2. All cultures were positive for HVS antigens, infectious centers, or DNA.' The reactivity of monoclonal antibodies to cell surface markers suggested that the resultant cell lines were comprised of activated T cells. The properties of the in vitro-transformed cells were similar to those of cells established from HVS-induced owl monkey tumors. Our results suggest that infection of T lymphocytes with HVS results in decreased dependence of T cells upon exogenous IL-2 for growth.Herpesvirus saimiri (HVS) is a horizontally spread T-cell tropic herpesvirus of squirrel monkeys. As such, it is a member of a large group of primate lymphotropic herpesviruses, which includes the B-cell tropic Epstein-Barr virus (EBV) of man, the EBV-like viruses of Old World monkeys and apes, and the T-cell tropic viruses of New World monkeys (1). HVS is not pathogenic for squirrel monkeys but is potently oncogenic for several other species of New World monkeys and rabbits, where it produces fatal T-cell lymphomas and leukemias (2-8). Although HVS readily produces T-cell (11,12).Previous attempts to transform lymphocytes by cocultivation with HVS producer lymphocytes or by exposure to cellfree HVS have, with the rare exception noted above, been unsuccessful (refs. 3 and 13; unpublished results). Recently, cell lines were established with the aid of IL-2 from owl monkeys bearing HVS-induced tumors (14, 15). These cell lines are not dependent on IL-2 for growth and survival as are normal T cells but respond to it strongly in terms of increased cell growth. Based on this observation and the failure of previous in vitro transformation attempts made without IL-2, it was reasonable to assume that HVS transformation in vitro might also be aided by IL-2. Therefore, a transformation protocol was established in which cells were first activated by phytohemagglutinin (PHA) to induce IL-2 receptors and then were expanded in IL-2-containing medium prior to exposure to virus. The cells were then exposed to HVS and further cultured in IL-2-containing medium prior to 'testing them for IL-2-independent growth, the criterion used for transformation. In this paper we report the establishment and characterization of a series of cell lines established in vitro by HVS transformation of owl monkey lymphocytes. A preliminary account of these result...

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mentioning

confidence: 99%

Transformation of owl monkey T cells in vitro with Herpesvirus saimiri.

Rabin¹,

Hopkins²,

Desrosiers³

et al. 1984

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

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“…This analysis showed no differences in the envelope coding region, even under the most stringent (70% formamide) spreading conditions, thus strengthening the hypothesis on the relationship of F-MCF, SFFVp, and SFFVa. Furthermore, the heteroduplexes of the SFFVs to F-MCF showed unambiguously that no additional large substitutions, i.e., viral oncogenes (15,19), are present in SFFVP or SFFV,a that could account for the differences in their leukemogenicity.…”

Section: Discussionmentioning

confidence: 93%

“…Mammalian transforming retroviruses can be classified into two broad categories: those that have acquired rapid oncogenic potential through deletion of viral genes (gag, pol, or env) and recombination with one of a number of cellular oncogenes (15,19), and those that are viral env gene recombinants (6,8,11,17,32). Viruses in the first category are capable of rapidly transforming cells in vivo or in vitro.…”

Section: Discussionmentioning

confidence: 99%

Heteroduplex analysis of molecular clones of the pathogenic Friend virus complex: Friend murine leukemia virus, Friend mink cell focus-forming virus, and the polycythemia- and anemia-inducing strains of Friend spleen focus-forming virus

Gonda¹,

Kaminchick²,

Oliff³

et al. 1984

J Virol

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The pathogenic Friend virus complex is of considerable interest in that, although members of this group are genetically related, they differ markedly in biochemical and biological properties. Heteroduplex mapping of molecular clones of the Friend virus complex, which includes the replication-competent ecotropic Friend murine leukemia virus (F-MuLV) and mink cell focus-forming virus (F-MCF) and replication-defective polycythemiaand anemia-inducing strains of spleen focus-forming virus (SFFVp and SFFVa, respectively), was employed to provide insight into the molecular basis of their relationships. In heteroduplexes of F-MuLV x F-MCF, a major substitution of 0.89 kilobases in the env gene of F-MCF was discerned. Heteroduplexes of SFFVp x F-MuLV or F-MCF and SFFVa x F-MuLV or F-MCF showed several major deletions in the pol gene region and a single major deletion in the 3' half of the env gene region of SFFVp and SFFVa. A major substitution of 0.89 kilobases was mapped to the 5' end of the env deletion of SFFVp and SFFVa in heteroduplexes with F-MuLV, similar to that seen in F-MuLV x F-MCF heteroduplexes. In contrast, this env gene region was totally homologous in F-MCF x SFFVp or SFFVa and SFFVp x SFFV. heteroduplexes. Our results suggest that (i) both SFFVp and SFFVa lack part of the env gene at its 3' end, corresponding to the p15(E) coding region, (ii) major deletions occur in the pol and env genes which account for the replication defectiveness of SFFVp and SFFVa, (iii) minor substitutions occur in the gag gene region of SFFVa that are not present in SFFVp, F-MuLV, or F-MCF, (iv) a major substitution exists in the gp7O region of the env gene between F-MuLV and F-MCF that probably accounts for the differences in their host range specificities, (v) this substitution in F-MCF is identical to the gp7O part of the gp52 coding region of SFFVp and SFFVa, and (vi) heteroduplexes to F-MCF show unambiguously that no additional large substitutions are present in SFFVp or SFFVa that could account for differences in their leukemogenicity. The original isolate of Friend virus described in 1957 caused acute erythroblastosis associated with anemia (13). Passage of this Friend virus stock in several laboratories has resulted in the identification of several pathogenic strains that differ in their biological and biochemical properties (for a review, see reference 44). For example, Axelrad and Steeves (2) and Mirand et al. (24) described strains of Friend virus that caused polycythemia in susceptible mice, rather than anemia as originally described (13). Although all of these "strains" produce rapid erythroid proliferation, erythroleukemia, splenomegaly, and splenic foci, they can be distinguished by diagnosis of the terminal stages of their disease as being accompanied by polycythemia or anemia (2, 13, 24, 37, 44). The polycythemia and anemia strains of the Friend virus complex are each composed of at least two distinct viral components: (i) a replication-competent, ecotropic helper type C virus (F-MuLV) (23, 26, 38, 43, 45, 46) a...

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“…However, assessing an infectious etiology can be difficult (99) because of 1.-subclinical infections are common and this may lead to misclassification bias; 2.-complex interactions can result because many sexually transmitted infections do occur simultaneously; 3.-the presence of a latency period between exposure and outcome, which vary considerably; 4.-clinical follow-up studies always remain inconclusive (98,103,104,(106)(107)(108)(109). It was well known and established that the human papillomavirus (HPV) is the principal etiological agent in cervical neoplasia (103,(110)(111)(112)(113)(114)(115)(116)(117)(118), some other sexually transmitted organisms may either contribute to or protect against cervical carcinogenesis (70,72,119,120).…”

Section: Chlamydia Trachomatis De-regulated and Damage Host Dnamentioning

confidence: 99%

Chlamydia trachomatis. Co-factor or factor in cancer of the cervix?

Núñez-Troconis

2021

Invest Clin

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The objective of this article was to review and to analyze the possible role that Chlamydia trachomatis has as a co-factor in the origin and development of cervical cancer. For that purpose, the Latin-American and international bibliography was reviewed using the Pub-Med, Google Scholar, Springer, the Cochrane Library, Embase, Scielo, Imbiomed-L, Redalyc and Latindex databases. The searches included the key words: Chlamydia trachomatis, epidemiology of Chlamydia trachomatis, epidemiology of cervical cancer, Chlamydia trachomatis and infection, Chlamydia trachomatis and inflammation mechanisms, cervical cancer and co-factors, sexually transmitted infections and cervical cancer, cancer and inflammation mechanisms, carcinogenesis, inflammation mechanisms. Publications from 1970 to June 2020 were reviewed and analyzed. This review article analyzes the possible mechanisms that Chlamydia trachomatis could play in the carcinogenesis of the cervical cancer as a co-factor with the human papilloma virus or as an independent factor.

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Mechanisms of Viral Tumorigenesis

Cited by 8 publications

References 214 publications

Transformation of owl monkey T cells in vitro with Herpesvirus saimiri.

Transformation of owl monkey T cells in vitro with Herpesvirus saimiri.

Heteroduplex analysis of molecular clones of the pathogenic Friend virus complex: Friend murine leukemia virus, Friend mink cell focus-forming virus, and the polycythemia- and anemia-inducing strains of Friend spleen focus-forming virus

Chlamydia trachomatis. Co-factor or factor in cancer of the cervix?

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