Hendra virus (HeV) causes severe infection in a broad range of species leading to mortality in both humans and animals. Productive HeV infection occurred in wild type and mice deficient in interferon signalling (the body’s antiviral defence mechanism). But, unlike other animal species susceptible to HeV infection severe disease did not develop. Therefore the restriction of fulminating disease cannot be attributed solely to the efficacy of mouse interferon signalling pathways against HeV-mediated anti-interferon mechanisms. Little neutralising antibody response was seen, suggesting an innate response mechanism remains relevant to limiting the systemic effects of infection. IFITM proteins were possible candidates but replication and cytopathic effect continued in their presence.
|Qualification||Doctor of Philosophy|
|Award date||08 Jun 2018|
|Publication status||Published - 2018|