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J. Virol. doi:10.1128/JVI.01571-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Inhibitory effect of IFN- on BK virus gene expression and replication

Department of Microbiology and Immunology, and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA

^* To whom correspondence should be addressed. Email: imperial{at}umich.edu.

	Abstract

BK virus (BKV) is widely accepted to be the causative agent of polyomavirus nephropathy. In immunocompromised individuals, especially kidney transplant recipients, BKV can replicate in kidney epithelial cells, causing loss of renal function and eventual destruction of the graft. Advances in immunosuppressive therapies may be partially responsible for the increasing incidence of polyomavirus nephropathy among transplant recipients by more effectively eliminating components of the immune system, such as IFN--producing lymphocytes, that keep BKV infections at a subclinical level. In this study, we investigated the role of IFN- in regulating lytic infection by BKV. Treatment with IFN- inhibited the expression of the viral early protein, large tumor antigen (TAg), and the late protein, VP1, in a dose-dependent manner. We detected a 1.6- and 12-fold reduction in TAg transcripts at 48 and 96 hours post-infection, respectively, with 250 U/ml IFN- treatment, suggesting that IFN--mediated inhibition occurs at the level of transcription. Furthermore, IFN- inhibited the level of viral progeny production by as much as 50-fold at an MOI of 0.5 and 80-fold at an MOI of 0.1. The inhibitory effect of IFN- was similar for three different strains of BKV examined. These results indicate an important role for IFN- in regulating BKV lytic infection.