Literature DB >> 10343074

Herpesvirus saimiri as a model for gammaherpesvirus oncogenesis.

J U Jung1, J K Choi, A Ensser, B Biesinger.   

Abstract

Herpesvirus saimiri (HVS) causes T-lymphoproliferative dis-$borders in several New World and Old World primate species and in certain rabbits.In vitro infection leads to permanent growth of primary T cells of primate and human origins. The transformation-relevant proteins of HVS interact with cellular proto-oncoproteins which results in cell growth transformation. In addition, virus-encoded cellular homologues may contribute to transformation or persistence of HVS by altering cellular signal transduction and deregulating cell growth control. Because of the presence of a permissive cell culture system and in vitro Land in vivo transformation assays, HVS provides a unique opportunity to investigate the mechanisms of cancer induction by oncogenic herpesviruses. Copyright 1999 Academic Press.

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Year:  1999        PMID： 10343074     DOI： 10.1006/scbi.1998.0115

Source DB:  PubMed          Journal:  Semin Cancer Biol        ISSN： 1044-579X            Impact factor:   15.707


  40 in total

Review 1.  Signaling activities of gammaherpesvirus membrane proteins.

Authors:  B Damania; J K Choi; J U Jung
Journal:  J Virol       Date:  2000-02       Impact factor: 5.103

2.  Murine gammaherpesvirus 68 cyclin D homologue is required for efficient reactivation from latency.

Authors:  A T Hoge; S B Hendrickson; W H Burns
Journal:  J Virol       Date:  2000-08       Impact factor: 5.103

3.  Gammaherpesvirus lytic gene expression as characterized by DNA array.

Authors:  Joo Wook Ahn; Kenneth L Powell; Paul Kellam; Dagmar G Alber
Journal:  J Virol       Date:  2002-06       Impact factor: 5.103

4.  The collagen repeat sequence is a determinant of the degree of herpesvirus saimiri STP transforming activity.

Authors:  J K Choi; S Ishido; J U Jung
Journal:  J Virol       Date:  2000-09       Impact factor: 5.103

5.  Herpesvirus saimiri vFLIP provides an antiapoptotic function but is not essential for viral replication, transformation, or pathogenicity.

Authors:  D Glykofrydes; H Niphuis; E M Kuhn; B Rosenwirth; J L Heeney; J Bruder; G Niedobitek; I Müller-Fleckenstein; B Fleckenstein; A Ensser
Journal:  J Virol       Date:  2000-12       Impact factor: 5.103

6.  Gammaherpesvirus gene expression and DNA synthesis are facilitated by viral protein kinase and histone variant H2AX.

Authors:  Bryan C Mounce; Fei Chin Tsan; Lindsay Droit; Sarah Kohler; Justin M Reitsma; Lisa A Cirillo; Vera L Tarakanova
Journal:  Virology       Date:  2011-09-22       Impact factor: 3.616

Review 7.  Immune evasion by Kaposi's sarcoma-associated herpesvirus.

Authors:  Hye-Ra Lee; Stacy Lee; Preet M Chaudhary; Parkash Gill; Jae U Jung
Journal:  Future Microbiol       Date:  2010-09       Impact factor: 3.165

8.  Kaposi's sarcoma-associated herpesvirus-encoded latency-associated nuclear antigen modulates K1 expression through its cis-acting elements within the terminal repeats.

Authors:  Subhash C Verma; Ke Lan; Tathagata Choudhuri; Erle S Robertson
Journal:  J Virol       Date:  2006-04       Impact factor: 5.103

9.  Gamma-herpesvirus kinase actively initiates a DNA damage response by inducing phosphorylation of H2AX to foster viral replication.

Authors:  Vera L Tarakanova; Van Leung-Pineda; Seungmin Hwang; Chiao-Wen Yang; Katie Matatall; Mickael Basson; Ren Sun; Helen Piwnica-Worms; Barry P Sleckman; Herbert W Virgin
Journal:  Cell Host Microbe       Date:  2007-06-14       Impact factor: 21.023

Review 10.  Molecular biology of Kaposi's sarcoma-associated herpesvirus and related oncogenesis.

Authors:  Qiliang Cai; Suhbash C Verma; Jie Lu; Erle S Robertson
Journal:  Adv Virus Res       Date:  2010       Impact factor: 9.937
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