In our preliminary studies, it was shown that CedPV was able to replicate in guinea pigs and ferrets, but failed to cause significant clinical diseases, unlike that of the closely related HeV and NiV. These first infection experiments were conducted with a high dose if virus to establish whether the CedPV could replicate in these animals and determine the degree of any clinical disease. A second experiment was then carried out in ferrets to determine the site of replication and tissue tropism in sequentially sacrificed animals. A lower dose was used to gain better comparison with similar infection experiments using HeV and NiV [18, 35] . Although these initial experimental infection studies indicate that CedPV is less or non-pathogenic in these species, it is possible that CedPV may be pathogenic in other hosts, such as horses. We hypothesize that the lack of a V protein may impact on the pathogenicity. In this regard, it was encouraging to observe that infection of human cells by CedPV induced a much more robust IFN-b response than HeV. Further study is required to dissect the exact molecular mechanism of this observed difference. Due to the close relationship between CedPV and HeV, it was important to investigate the possibility of co-infection by these two viruses in the Australian bat population. Based on the detection of neutralizing antibodies at 23% for CedPV, 37% for HeV and 8% for both, it can be concluded that the co-infection rate is very close to the theoretical rate of 8.5% (the product of the two independent infection rates). Based on this limited preliminary analysis, it appears that infection of bats by one henipavirus neither prevents nor enhances the likelihood of infection by the other.