I’m a rabbit ecologist and biological control expert. I have worked on aspects of rabbit control for over 50 years including the introduction of rabbit fleas as myxomatosis vectors and bringing rabbit haemorrhagic disease virus (RHDV or calicivirus) into Australia to further deal with the rabbit problem. Ask Me Anything about this area of research and I'll try to find the answer!! As Patron of of Rabbit-Free Australia I am pleased to do what ever I can to help explore options for the control of rabbits and how to implement them. So again, please ask if you have any questions.

At the moment I'm reviewing all the past research literature on myxomatosis and its effects. Although it was first released among Australian rabbits over 70 years ago it has persisted and still has a powerful effect in reducing rabbit abundance. Furthermore, it has kept pace with growing rabbit disease resistance in a 'biological arms race' so that today's myxoma viruses are very lethal in domestic rabbits although killing only about 50% of wild rabbits. 

Although we know a lot about rabbits and myxomatosis it may be surprising for readers to know that none of this knowledge helps much in predicting what will happen with myxomatosis in the future. Since we released RHDV as a second biological control agent myxomatosis has broken out less frequently - but have rabbits begun to lose their resistance to the disease? Or are myxoma viruses becoming less powerful?

We simply do not know the answer to these questions and further research could give useful answers! 

Immunocontraception, better referred to as virally-vectored immunocontraception or VVIC, was based on the idea that rabbit genes that produced coat-proteins for rabbit ova could be inserted into a myxoma virus. If female rabbits were infected with this genetically modified virus and recovered, they would not only form antibodies against the virus but also against their own ova, making them sterile.

In fact, the idea initially worked in the CSIRO laboratory. A modified myxoma virus was 'constructed' and female rabbits infected with the virus were infertile. However, the rabbits soon lost the antibodies produced against their ova proteins and gradually became fertile again. Furthermore, as suggested, the modified myxoma virus was unlikely to compete well enough with naturally circulating viruses in the field to infect most of the female rabbits in wild populations. Field experiments where female rabbits were surgically sterilized suggested that about 80% of female rabbits would need to be infertile to drive rabbit abundance down. 

So, as a very humane form of rabbit control it seemed promising, but there were too many barriers to make it practical for field use and after almost 14 years of hard work CSIRO abandoned the project in the early 2000s.

Hi Jarvis,

It is not inevitable that viruses like myxoma virus (MYXV) or rabbit haemorrhagic disease virus (RHDV) will eventually become less effective because they naturally become less virulent or because of increased resistance or immunity in rabbits.

This is because virulence is selectively adjusted, maximizing transmissibility, as the rabbit host develops greater resistance. The final outcome can depend on the genetic capacity of the virus to match or avoid host defences. In the case of myxoma virus, a large DNA virus, it has the capacity to supress the rabbit's immune system, hence it has been increasing in virulence as rabbits become more resistant. Today’s myxoma viruses appear to have kept pace with increases in rabbit resistance and still kill about 50% of wild rabbits just as they did 30 - 40 years ago.

On the other hand, RHDV, which is a small RNA virus, simply gets in and replicates rapidly before the rabbit’s immune system can react. It kills about 70% of infected rabbits. We think that, by killing rabbits, the chances of its spread by blowflies is increased. By contrast, non-pathogenic RCV-A1, although closely related to RHDV, effectively presents a small target by confining infection to a few gut cells. It causes no illness and does not strongly stimulate the rabbit's immune system. That way it can quietly replicate over a longer period and virus particles are excreted in rabbit faeces enabling the virus to spread. Presumably, rabbits stand on virus contaminated faeces and when they groom, which involves licking their paws, they ingest RCV-A1 viral particles.

The different ‘strategies’ for virus persistence that have evolved are varied and well understood but we can’t really predict what will happen in the long run. For example, contrary to what one might expect, highly lethal RHDV is thought to have evolved from a non-pathogenic precursor like RCV-A1. We can therefore say that it is not inevitable that viruses will always attenuate and become less effective.

Because myxomatosis has been effective in killing a substantial proportion of the rabbits it infects for over 70 years and RHDV has been around for 25 years (partly replaced by RHDV2) and causes even higher mortality, we can probably assume that both viruses will continue to be useful biological control agents for many years to come.