This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tarakanova, V. L.
Right arrow Articles by Virgin, H. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tarakanova, V. L.
Right arrow Articles by Virgin, H. W., IV

 Previous Article  |  Next Article 

Journal of Virology, January 2008, p. 1034-1039, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01426-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Murine Gammaherpesvirus 68 Genes both Induce and Suppress Lymphoproliferative Disease{triangledown}

Vera L. Tarakanova,1,{dagger} Friederike Kreisel,1,{dagger} Douglas W. White,1,2 and Herbert W. Virgin IV1,3*

Department of Pathology and Immunology,1 Department of Internal Medicine, Division of Rheumatology,2 Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 631103

Received 29 June 2007/ Accepted 23 October 2007

Gammaherpesvirus infection is associated with an increased incidence of lymphoproliferative disease in immunocompromised hosts. Murine gammaherpesvirus 68 ({gamma}HV68) infection of BALB β2-microglobulin-deficient (BALB β2m–/–) mice provides an animal model for analysis of the mechanisms responsible for the induction of a lymphoproliferative disease, atypical lymphoid hyperplasia (ALH), that is pathologically similar to posttransplant lymphoproliferative disease associated with Epstein-Barr virus infection. Here we report that the {gamma}HV68 v-cyclin and v-bcl-2 genes are required for the efficient induction of {gamma}HV68-associated ALH in BALB β2m–/– mice, while the v-GPCR gene is dispensable for ALH induction. In contrast to these findings, deletion of the viral M1 gene enhanced ALH. Thus, {gamma}HV68 genes can either inhibit or enhance the induction of lymphoproliferative disease in immunocompromised mice.

* Corresponding author. Mailing address: Department of Pathology and Immunology, Washington University, 660 S. Euclid Ave, Box 8118, St. Louis, MO 63110. Phone: (314) 362-9223. Fax: (314) 362-0369. E-mail: virgin{at}wustl.edu

{triangledown} Published ahead of print on 31 October 2007.

{dagger} V.L.T. and F.K. contributed equally to this study.

Journal of Virology, January 2008, p. 1034-1039, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01426-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Gredmark-Russ, S., Isaacson, M. K., Kattenhorn, L., Cheung, E. J., Watson, N., Ploegh, H. L. (2009). A Gammaherpesvirus Ubiquitin-Specific Protease Is Involved in the Establishment of Murine Gammaherpesvirus 68 Infection. J. Virol. 83: 10644-10652 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»