This model may be of particular value in studying aspects of recrudescence. In most other animal models of HeV infection, exposure rapidly leads to acute and fatal disease. In juvenile mice, we have observed that clinical disease may not develop (up to at least day 21 post exposure) despite strong evidence of viral replication in brain that is also continuing in the face of circulating antibody to G protein. Furthermore evidence of encephalitis in these animals was observed in the absence of vasculitis. Some of these characteristics are a feature of both recrudescent human HeV [1] and also NiV [41, 42] infection; the mouse HeV model could be employed to explore the mechanisms by which the potential for virus replication may be sustained in convalescent individuals.