Can we afford the risks of having, or of not having rabbit haemorrhagic disease (RHD) viruses? Debate is intensifying, but certainty is elusive. There are many questions, but few answers. The rabbits themselves, and one alleged solution - introduction of ferrets (that spread bovine TB) and their relatives - arose from ill-advised introductions. Are we about to repeat the process?

Some farmers, often on poor, dry lands have had rabbit problems since the "rabbit boards" were abolished. Dependant on subsidies, the boards effectively controlled rabbits. But subsidies are unfashionable. Where rainfall is higher, rabbits are usually controlled by a disease (coccidiosis) and by cats. Rabbits are not a national problem. D. E. Wright's recent research paper concluded that the national cost of rabbits does not justify a major research effort. Locally rabbits are out of control. Control costs are high, and farmers want help. Biological control agents have been welcomed, but without appreciating the issues involved. Myxomatosis fell from favour as its effectiveness declined, and horror of the puss-laden lesions increased. Rabbit haemorrhagic disease (RHD) sounded more attractive, because lethal internal bleeding or clotting would not be seen by the public. To minimise public abhorrence the Australians re-named it Rabbit Calicivirus Disease (RCD) hoping to avoid linkage with human haemorrhagic disease (Ebola).

RHD first appeared in China in 1984 where it killed about 90% of farmed rabbits. Its original host remains unknown. Rabbits were new hosts. Dispersal to reach Spain in 1988 was too rapid to be explained by rabbit-to-rabbit transmission. Could birds be involved?, (They host some caliciviruses.) Methods of transmission remain uncertain: flies, and carnivore's faeces may have a role.

The virus's identity is in doubt- Chinese, Bulgarian and US labs have identified a parvovirus from diseased rabbits. Other labs in Europe and Australia have identified calicivirus. The best guess seems that many isolates are mixtures of at least two kinds. Because the Australians have worked with a single fraction of the Czech isolate, they may have overlooked the heavier parvovirus. The application is to import the Czech "isolate" of calicivirus, but its purity, and the variety(s) of RCV contained is unknown. The crude myxoma virus used in Southland and Queensland in the early 1950s- which some associate with the appearance of ME or Tapanui flu. makes certainty about virus identity an important, but unaddressed issue. Uncertainties here can cloud the issues of human health implications, efficiency in rabbit control, and environmental effects.

Myxomatosis no longer controls rabbits because many are immune, and the virus has diminished virulence. This is normal for pathogens in this kind. Myxoma is a DNA virus. Calicivirus is an RNA virus, and is thus about one million times more likelv to mutate than DNA viruses. Young rabbits are reportedly naturally immune to RHD. Because rabbit placentas are extremely intimate, antibodies pass readily from mother to foetus. This passive immunity is typically short-lived, but is reinforced via lactation. Whether active (life-long) immunity can be generated during burrow life through kits ingesting virus contaminated soft faeces from their mothers seems not to have been considered. (Food naturally passes twice down a rabbit's gut.)

Typically, passage of a lethal virus through a naive population leaves immune and dead hosts.

If the virus has no alternative host it dies out. If virus and host persist for a period (as myxoma has) typically some accommodation is reached, with increasing immunity, and decreasing mortality (or virulence). It must be expected that control of rabbits will be short-lived, and of decreasing effectiveness. A recent Spanish report stated that when RHD first appeared in 1988 rabbit mortality was about 90%. By late 1995 mortality in different areas ranged between 2 and 30%. Reports of Australian experience vary from a common initial kill of about 90% to insignificant, though in some areas myxoma immunity seems to reduce RHD's efficacy. There is no reason to think that in New Zealand control will be total or enduring.

Parasites may produce different symptoms in different hosts. Plague is benign in many rodents, but often lethal to man. AIDS (another RNA virus) lives quietly in monkeys, but not in man. Host specificity is a problem. Will the RHD virus stick with rabbits alone? No-one knows. RNA viruses are inherently unstable. Host switching, or extending host range is fairly common in viruses. The movement of AIDS and Ebola from monkeys to humans are recent examples. Knowledge of viral host ranges is usually incomplete. Many viruses are symptomless, and poorly known, so their presence is easily overlooked. San Miguel Sea Lion Virus (another calicivirus) is illustrative. First known in Eastern Coast swine, and later in cattle, it produces blisters around the mouth as in foot and mouth disease - hence the research, and our knowledge of it. Very common in North Pacific marine mammals, this virus entered pigs fed fish offals. Some birds (e.g. fairy terns in Hawaii) carry caliciviruses or antibodies to them. We do not know the host range of the RHD viruses. The tests on kiwis were severely criticised by other virologists and pathologists as unsatisfactory. They are not reliable. There is no knowledge of which native animals could be infected with RHD. Sea birds have not been tested or examined for antibodies. Without such knowledge the direct risks to wildlife are unassessable.

Human health implications are crucial. Acting on reports from independent virologists, the Ministry of Health concluded that it would not support the introduction of the virus. Dr Cherry's appropriate re-interpretation of Australian data on human health impacts disclosed a three-fold increase in gastro-intestinal upsets, flu-like symptoms and rashes in people heavilv exposed to the virus over controls. This cannot be ignored. The search for evidence of impact on people has been minimal. Difficulties in finding suitable control groups, and in interpreting the "background noise" without a massive research effort are inhibitory.

Environmental impacts of RHD need careful assessing. If RHD kills 90% of rabbits, then predators and scavengers will face first a glut of virus laden food, and then starvation. They will then eat whatever they can. Birds, lizards, insects will be oppressed. Some may be eliminated. Prey switching is inevitable. Poisoning reduces predators along with rabbits through secondary poisoning. Vegetation will change.

Consequences for trade and our "clean green image" need consideration. The US lists RHD as a Foreign Animal Disease which must be kept out. How? Bringing RHD for the first time into the roaring forties, and into the westwind drift system that encircles the southern oceans could be disastrous for others. These winds are ridden continuously by the albatross and petrel family of birds. With RHD in our region there is a grave risk that it will be dispersed down-wind by oceanic birds to South America, and perhaps to southern Africa. Once ashore, RHD could infect new rodents and birds and disperse northwards. Can we afford to risk the diplomatic and trade consequences of such effects?

Other costs include permanent loss of the chance to harvest the last large, virus-free feral rabbit population. Who will compensate present harvesters for their losses? Domesticated and farmed rabbits will need protection. The average Australian cost of vaccination which is not 100% effective, and has bad side-effects, is $A20 per rabbit. Protecting laboratory colonies needed for research and medical antibody work will be necessary and costly

I have read the nearly 800 submissions. Non-MAF scientists are gravely concerned. There is no commitment anywhere to ensuring that the releases are carried out in a properly controlled fashion, or that its effects are measured against reliable base-line data. Much informed counsel has been denigrated and scorned. Many fear we are in danger of approving an irresponsible, and uncontrolled adventure in biological warfare whose consequences are unpredictable. Too often absence of evidence is regarded as evidence of absence. No cost:benefit analysis is available. Is pastoral farming on these lands economically or environmentally sustainable? Do the returns pay for current infrastructure?