Mice were anaesthetised and exposed to a low passage clinical isolate of HeV (Hendra virus/Australia/Horse/2008/Redlands) [44] by either the intranasal or subcutaneous route. For the intranasal route, five aged (12 months) and five juvenile (8 weeks) Table 6 . Distribution of histologic lesions and viral antigen in the brain of intranasally HeV challenged mice. mice were anaesthetised, placed in dorsal recumbency and exposed to 50,000 TCID 50 in 50 ml saline by slow drop application to the nares. For the subcutaneous route, five aged and five juvenile mice were anaesthetised and exposed to 50,000 TCID 50 virus in 200 ml saline by subcutaneous injection. Animals were monitored daily thereafter and euthanased when reaching a previously determined end-point or at 21 days post infection (pi). The humane end-point was defined as a constant weight loss recorded over 3 days or reaching a 20% loss of pre-infection weight, and/or clinical signs consistent with neurological involvement including ataxia, tremors, depression and behavioural changes. As clinical signs of Hendra infection have not been observed in mice previously, the pre-determined endpoint was modelled on infection outcomes recorded for guinea pigs.