Rabbit haemorrhagic disease was introduced onto the Australian mainland in 1995.  It has since spread to most regions where rabbits exist but its effectiveness varies between regions.  Generally, it is more effective in arid regions and patchy or ineffective in wetter areas.  The reasons for this are not known but it could be related to, for example, vector type and abundance, survival of the virus in wetter conditions, rabbit population dynamics, and/or the presence of other infectious agents.

There is good serological evidence that there is another calicivirus or caliciviruses circulating in the Australian wild rabbit population and that this virus, or viruses, was present prior to the release of RHDV.  This virus is serologically related to RHDV but its influence on the epidemiology of RHDV has not been determined.

Elimination of RHDV-like infection as a factor influencing the effectiveness of RHD in Australia is important in our quest to understand why RHD works better in some areas and not others.

Knowledge about the epidemiology of different viruses naturally infecting rabbits may also be critical information in determining the timing of bait delivered RHDV.

So far the only evidence of the existence of these RHD-like viruses is serological, tha actual infectious agent has never been detected. While serology is an excellent tool to monitor infection history, it does not necessarily allow to detect an active infection.

In case of a short-lived infection, the virus may be long cleared from the organism by the time detectable antibodies are developed. Long term studies monitoring the change of antibody patterns to the putative benign virus in rabbit populations show that young rabbits are most likely to become infected between 6 and 12 weeks of age. This project therefore targets young rabbits from sites that have higher than average rainfall and/or a known history and high incidence of the putative benign virus.

Outcomes