Hendra virus and Nipah virus are closely related paramyxoviruses that naturally exist in pteropodid bats. Spill-over events from the natural animal reservoir have led to clinical disease in several mammalian species including humans. Infection in humans initially presents as an influenza like illness that can and often does progress to fatal encephalitis. Despite encephalitis being the most serious sequelae of infection with these viruses little is known of their neuropathogenesis. Recently our laboratory identified a new mouse model of Hendra virus infection that is particularly useful for studying the encephalitic component of the disease. We found that aged mice reliably developed clinical encephalitic disease following intranasal exposure to Hendra virus. Encephalitis developed in the absence of viremia or systemic disease suggesting a route of entry to the brain that was other than haematogenous. Immuno- histopathological examination of sequential transverse brain and nasal cavity sections from mice euthanased at two daily intervals suggested that Hendra virus enters the brain at the olfactory bulbs along olfactory sensory neurons from the nasal cavity, and continues to higher order centers of the brain along components of the olfactory pathway. The confinement of virus to neurons, and the directional rather than radial pattern of spread within the brain, suggests that viral movement is confined to synaptically connected chains of neurons. Taken together, these studies report a new animal model of Hendra virus encephalitis that offers great promise in contributing to knowledge of Hendra virus neuropathogenesis. The studies also reveal a mechanism of neuroinvasion along olfactory receptor neurons that has not been described for Hendra virus previously. This is valuable information for the development of improved treatment options for human cases of disease.