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Nature: a Selective Approach

More sharply than ever before, myxoma virus is posing ethical problems and challenging simplistic attitudes as to what we think of as "natural"

Bernard Dixon

Do we want rabbits to suffer and die from myxomatosis? Or should we seek instead to protect them against such a grotesque, disfiguring, painful disease? In the case of other pathogens and hosts, such questions might appear to be callously superfluous. Myxoma virus, however, presents a genuine dilemma. Though not wholly new, the perplexity has been sharpened considerably by myxomatosis vaccine research in Spain which threatens pest control in Australia. The conundrum is one of many that ought to attract the attention of all those (like the heir to the British throne) who want to believe in a natural world that is pristine, pleasant, and morally unambiguous.

Genetic modification is the ingredient giving new, tantalizing significance to an infection which was first deliberately introduced into Australia and Europe in the early 1950s. I well recall from that time my own horror when I stumbled over two rabbits dying of the disease as I walked through a riverside field in northern England.

Modern knowledge of this ghastly virus infection—which is characterized by horrible mucilaginous tumors on the skin—dates from just before the turn of the century. In 1895, the government of Uruguay invited Guiseppi Sanarelli, a microbiologist at the University of Siena, to set up an institute of hygiene at Montevideo. Sanarelli accepted, and in the course of establishing the new center he introduced European domestic rabbits to Uruguay for the first time. They were needed for producing sera containing antibodies against various diseases. The following year, however, the rabbits developed the extremely infectious and lethal disease, then unknown in Europe, which we now call myxomatosis. Nearly half a century elapsed before the common wild rabbit of Brazil was incriminated as the carrier of the myxoma virus, and before the method of transmission, via mosquito bites, was firmly proved. Mosquitoes also convey the disease in Australia and parts of Europe. Rabbit fleas are the major vector in Britain.

Because the European wild rabbit is a major pest in Australia, agriculturalists tried repeatedly to establish the myxomatosis virus there. But they did not succeed until 1950, when infected rabbits were introduced into the Murray Valley. The splendid weather that summer and in the following two years provided unusually favorable conditions for mosquitoes to breed and travel far. Myxomatosis spread like wildfire. Millions of rabbits—about four-fifths of those in southeastern Australia—succumbed.

Myxomatosis was introduced into France in June 1952, and by the end of the following year it had reached Belgium, Luxemburg, Germany, the Netherlands, and Spain. The first outbreaks in Britain were in the southern county of Kent, and the disease moved so rapidly that by the end of 1955 well over nine-tenths of the rabbits in the country were dead.

Yet Britain's rabbit population later began to thrive again. Today, the animals are again considered a serious pest and a significant factor in agricultural economics. In Australia, the disease remains important in regulating the rabbit population.

There have, however, been two significant changes since the first efforts at biological control. The first alteration was in the virulence of the myxoma virus. The lethal organism first introduced into Australia killed over 99% of infected rabbits. Yet within 12 months, strains had appeared with a mortality rate of only 90%. In subsequent years even milder strains nave prospered, in some cases having mortality rates as low as 20%. The explanation, as the Australian virologist Macfarlane Burnet observed long ago in Biological Aspects of Infectious Disease (Cambridge University Press, 1940), is simply that there is little point in a microorganism destroying its host in spectacular fashion if this leaves it with no prospect of being ferried to other vulnerable hosts. The chances of further transmission are much greater for a virus that is comparatively mild, and which therefore produces a lengthier disease and infectious period, than with one that kills its host rapidly.

As Charles Darwin might have predicted, rabbits have changed too. Under the rigorous pressures of regular exposure to a myxoma virus that was highly lethal, resistant strains emerged. During a seven-year period in Australia resistance increased to such a degree that a virus that originally killed 90% of wild rabbits would eventually destroy only some 30% or so.

The work by Frank Fenner and his colleagues on the coevolution of rabbits and myxoma viruses in Australia in the 1950s and 60s is one of Australia's great contributions to microbiology. From that research, two major lessons emerged. First, the conditions for successful microbiological control of a ``pest'' population are so complex that initial failures need have little significance for the eventual outcome of a project.

Second, genetic changes in both the microbial and host populations can quickly alter the ground rules—though the extent to which this happens will depend on environmental factors and on intelligent anticipation. Above all, the long-term success of biological control rests on a thorough understanding of the spread and persistence of disease in natural populations.

And now we have a new myxoma virus, genetically modified by Juan Torres and his colleagues at the Center for Investigation into Animal Health in Madrid, Spain. It is not only attenuated, so that it immunizes rabbits against myxomatosis. It also carriers a gene coding for a protein from rabbit hemorrhagic disease (RHD) and thus confers immunity against this killer too. The virus (which is being tested in a population of 300 rabbits on a small island) has been disabled so that it can spread from one rabbit to another for one generation only. The question is: do we really want to protect rabbits against these two lethal infections? However strange the question might appear if applied to other diseases, here it poses genuine difficulty because of the differing perspectives of two different countries.

In Spain, populations of rabbits are sparse. Indeed, Juan Torres claims that myxomatosis and RHD are endangering the survival not only of rabbits but also of their natural predators. In this context, a vaccination initiative can be seen as a conservation measure as important as efforts to protect elephants in Africa or whales in the oceans.

In Australia, on the other hand, rabbits remain serious pests, especially for farmers, and the two infections play an important, "natural" role in restricting their numbers. If the new transgenic myxoma virus were to be released there by mistake, it could jeopardize the success of this biological control. While the organism's limited capacity for replication might seem to limit any danger, further genetic changes could make matters worse.

By ironic coincidence, it is evidence from work on the microbiological regulation of rabbit populations in Australia that provides the sharpest reminder of the risks inherent in such work. Just five years ago, a calcivirus, being considered as an additional agent to control rabbits, escaped to the mainland from the island where it was being field tested. Although millions of rabbits died as a result, this all happened before ecological questions (such as possible effects on other species) had been clearly answered.

The moral ambiguity of the challenges posed by a biological control agent such as myxoma virus is one thing. It is an altogether different matter to proceed with such a questionable initiative in an area where serious practical mistakes have already been made.

Last Modified: January 12, 2001
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