Abstract

The Epstein-Barr virus is the etiologic agent of infectious mononucleosis and is associated with Burkitt's lymphoma and nasopharyngeal carcinoma. This research project will study the gene regulation of the Epstein-Barr virus at the transcriptional level, and investigate possible interactions between the EBV and HIV viruses. To accomplish this goal, a representative promoter unit from each of the four types of EBV genes (latent, immediate- early, early and late) will be placed upstream of the bacterial CAT (chloramphenicol acetyl transferase) gene. The EBV-CAT vectors will then be used to ask such questions as whether any of the EBV promoters have tissue specific activity, whether there are EBV encoded promoters which function in trans to activate other EBV gene promoters, and whether the differential expression of latent versus non-latent genes is regulated interaction of the EBV and HIV viruses at the molecular level, since patients with AIDS have high frequency of EBV-associated lymphomas. Using CAT vectors containing either EBV or HIV promoters, we will investigate whether the HIV TAT protein is able to transactivate the EBV promoters, and likewise, whether EBV encoded proteins can transactivate the HIV promoter.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08CA001229-05
Application #
3079735
Study Section
Special Emphasis Panel (SRC (33))
Project Start
1987-02-01
Project End
1993-01-31
Budget Start
1991-02-01
Budget End
1993-01-31
Support Year
5
Fiscal Year
1991
Total Cost
Indirect Cost

  Institution

Name
University of North Carolina Chapel Hill
Department
Type
Schools of Medicine
DUNS #
078861598
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599

  Publications

Furnari, F B; Zacny, V; Quinlivan, E B et al. (1994) RAZ, an Epstein-Barr virus transdominant repressor that modulates the viral reactivation mechanism. J Virol 68:1827-36
Quinlivan, E B; Holley-Guthrie, E A; Norris, M et al. (1993) Direct BRLF1 binding is required for cooperative BZLF1/BRLF1 activation of the Epstein-Barr virus early promoter, BMRF1. Nucleic Acids Res 21:1999-2007
Zalani, S; Holley-Guthrie, E A; Gutsch, D E et al. (1992) The Epstein-Barr virus immediate-early promoter BRLF1 can be activated by the cellular Sp1 transcription factor. J Virol 66:7282-92
Kenney, S C; Holley-Guthrie, E; Quinlivan, E B et al. (1992) The cellular oncogene c-myb can interact synergistically with the Epstein-Barr virus BZLF1 transactivator in lymphoid cells. Mol Cell Biol 12:136-46
Holley-Guthrie, E A; Quinlivan, E B; Mar, E C et al. (1990) The Epstein-Barr virus (EBV) BMRF1 promoter for early antigen (EA-D) is regulated by the EBV transactivators, BRLF1 and BZLF1, in a cell-specific manner. J Virol 64:3753-9
Quinlivan, E B; Holley-Guthrie, E; Mar, E C et al. (1990) The Epstein-Barr virus BRLF1 immediate-early gene product transactivates the human immunodeficiency virus type 1 long terminal repeat by a mechanism which is enhancer independent. J Virol 64:1817-20
Kenney, S; Holley-Guthrie, E; Mar, E C et al. (1989) The Epstein-Barr virus BMLF1 promoter contains an enhancer element that is responsive to the BZLF1 and BRLF1 transactivators. J Virol 63:3878-83
Kenney, S; Kamine, J; Holley-Guthrie, E et al. (1989) The Epstein-Barr virus immediate-early gene product, BMLF1, acts in trans by a posttranscriptional mechanism which is reporter gene dependent. J Virol 63:3870-7
Kenney, S; Kamine, J; Holley-Guthrie, E et al. (1989) The Epstein-Barr virus (EBV) BZLF1 immediate-early gene product differentially affects latent versus productive EBV promoters. J Virol 63:1729-36
Pagano, J S; Kenney, S; Markovitz, D et al. (1988) Epstein-Barr virus and interactions with human retroviruses. J Virol Methods 21:229-39

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