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3231963 
Journal Article 
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 
Jinno-Oue, A; Wilt, SG; Hanson, C; Dugger, NV; Hoffman, PM; Masuda, M; Ruscetti, SK 
2003 
1 
Journal of Virology
ISSN: 0022-538X
EISSN: 1098-5514 
77 
9 
5145-5151 
English 
12692217 
WOS:000182297200013 
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.