Demyelination induced by mouse hepatitis virus (MHV), strain JHM, is in lar
ge part immune mediated, but little is known about the mechanisms involved
in this process. Previous results suggest that inducible nitric oxide synth
ase (NOS2) contributes transiently to MHV-induced demyelination, Herein, we
show that equivalent amounts of demyelination were evident at day 12 after
MHV infection in mice genetically deficient in NOS2 (NOS2(-/-)) and in C57
BL/6 mice. Furthermore, using an established adoptive transfer model and ph
armacological inhibitors of NOS2 function, we could demonstrate no effect o
n MHV-induced demyelination. These results indicate that NOS2 function is n
ot required for demyelination in mice infected with MHV.