Abstract
We have investigated the contribution of the interferon (IFN)-α/β system, IFN-γ and nitric oxide to recovery from infection with Murray Valley encephalitis virus, using a mouse model for flaviviral encephalitis where a small dose of virus was administered to 6-week-old wild-type and gene knockout animals by the intravenous route. We show that a defect in the IFN-α/β responses results in uncontrolled extraneural virus growth, rapid virus entry into the brain and 100 % mortality. In contrast, mice deficient in IFN-γ or nitric oxide production display an only marginally increased susceptibility to infection with the neurotropic virus.