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Murine gammaherpesvirus 68 genes both induce and suppress lymphoproliferative disease. J Virol 2008 Jan;82(2):1034-9

Date

11/06/2007

Pubmed ID

17977975

Pubmed Central ID

PMC2224605

DOI

10.1128/JVI.01426-07

Scopus ID

2-s2.0-37849044580   27 Citations

Abstract

Gammaherpesvirus infection is associated with an increased incidence of lymphoproliferative disease in immunocompromised hosts. Murine gammaherpesvirus 68 (gammaHV68) infection of BALB beta(2)-microglobulin-deficient (BALB beta(2)m(-/-)) 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 gammaHV68 v-cyclin and v-bcl-2 genes are required for the efficient induction of gammaHV68-associated ALH in BALB beta(2)m(-/-) 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, gammaHV68 genes can either inhibit or enhance the induction of lymphoproliferative disease in immunocompromised mice.

Author List

Tarakanova VL, Kreisel F, White DW, Virgin HW 4th

Author

Vera Tarakanova PhD Associate Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Cyclins
Lymphoproliferative Disorders
Mice
Mice, Inbred BALB C
Mice, Knockout
Proto-Oncogene Proteins c-bcl-2
Rhadinovirus
Viral Proteins
beta 2-Microglobulin
jenkins-FCD Prod-482 91ad8a360b6da540234915ea01ff80e38bfdb40a