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Infection of BALB\/c (H-2<jats:sup>d<\/jats:sup>) mice expressing a dominant negative gamma interferon (IFN-\u03b3) receptor specifically in oligodendrocytes was examined to determine the influence of IFN-\u03b3 signaling on pathogenesis. Inhibition of IFN-\u03b3 signaling in oligodendrocytes increased viral load, infection of oligodendrocytes, oligodendrocyte loss, demyelination, and axonal damage resulting in increased mortality. IFN-\u03b3 levels and the inflammatory response were not altered, although the level of tumor necrosis factor (TNF) mRNA was increased. 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