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Journal of Virology, May 2003, p. 5145-5151, Vol. 77, No. 9
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.9.5145-5151.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Expression of Inducible Nitric Oxide Synthase and Elevation of Tyrosine Nitration of a 32-Kilodalton Cellular Protein in Brain Capillary Endothelial Cells from Rats Infected with a Neuropathogenic Murine Leukemia Virus

Atsushi Jinno-Oue,^1, Susan G. Wilt,^2, Charlotte Hanson,¹ Natalie V. Dugger,² Paul M. Hoffman,² Michiaki Masuda,³ and Sandra K. Ruscetti^1*

Basic Research Laboratory, National Cancer Institute, Frederick, Maryland 21702,¹ Research Service, Department of Veterans Affairs Medical Center and Department of Neurology, University of Maryland, Baltimore, Maryland 21201,² Department of Microbiology, School of Medicine, Dokkyo University, Tochigi 321-0293, Japan³

Received 7 October 2002/ Accepted 4 February 2003

PVC-211 murine leukemia virus (MuLV) is a neuropathogenic variant of Friend MuLV (F-MuLV) which causes a rapidly progressive spongiform neurodegenerative disease in rodents. The primary target of PVC-211 MuLV infection in the brain is the brain capillary endothelial cell (BCEC), which is resistant to F-MuLV infection. Previous studies have shown that changes in the envelope gene of PVC-211 MuLV confer BCEC tropism to the virus. However, little is known about how infection of BCECs by PVC-211 MuLV induces neurological disease. Previous results suggest that nitric oxide (NO), which has been implicated as a potential neurotoxin, is involved in PVC-211 MuLV-induced neurodegeneration. In this study, we show that expression of inducible nitric oxide synthase (iNOS), which produces NO from L-arginine, is induced in BCECs from PVC-211 MuLV-infected rats. Furthermore, elevated levels of a 32-kDa cellular protein modified by 3-nitrotyrosine, which is a hallmark of NO production, were observed in virus-infected BCECs. BCECs from rats infected with BCEC-tropic but nonneuropathogenic PVF-e5 MuLV, which is a chimeric virus between PVC-211 MuLV and F-MuLV, fail to induce either iNOS expression or elevation of tyrosine nitration of a 32-kDa protein. These results suggest that expression of iNOS and nitration of tyrosine residues of a 32-kDa protein in PVC-211 MuLV-infected BCECs may play an important role in neurological disease induction.

Present address: Department of Virology and Preventive Medicine, Gunma University School of Medicine, Gunma 371-8511, Japan.

Present address: R & D Program 151, Department of Veterans Affairs Medical Center, Bronx, NY 10468.

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