Remember carp herpes? Or caaaaaaaaarp herpes, as then-deputy prime minister Barnaby Joyce put it back in 2016?
The piscatorial STD was meant to rid our waterways of arguably our worst aquatic pest.
At least, that was the impression you'd have gotten from Mr Joyce's performance in parliament at the time.
"It was great to be able to announce the $15 million we will put towards the eradication of carp," he said.
Although watching the recording of Mr Joyce again, his mind was maybe elsewhere.
"We are afflicted in this nation with these disgusting, mud-sucking creatures," he said, nodding toward the then-opposition, "for which the only form of control is a version of herpes ... "
Six years on, Mr Joyce is on the other side of the fence and Australian carp are blissfully unaware of his threat.
So where did the money go, and when, if ever, can we expect to see the virus released in our waterways?
Quick refresher: what is the virus?
Cyprinid herpesvirus 3 was first identified following a large outbreak at a carp farm in Germany in 1997, which was followed by similar outbreaks in the US and Israel the following year.
Infected fish were found blotched white, with patches of bleeding skin, necrosis or rotting of the gills, and showing signs of lethargy, among other symptoms.
The virus is mostly spread via contact, meaning fish in high densities are most at risk of transmission.
While that's bad news for aquaculture, it could be the Achilles heel for the pest in Australia, which schools in huge numbers during breeding and when waterholes are drying up.
The government's $15 million investment was sunk into the National Carp Control Plan to investigate just that.
Isn't biological control how we got cane toads?
Australians are generally a wary bunch when it comes to biological controls, probably thanks largely to the notorious cane toad.
But the introduction of the cane toad isn't a good parallel for how biological controls are done today, or even how they were meant to be done back in 1935.
There was virtually no research conducted into the potential ecological impacts of the cane toad, which was released here by an entomologist employed by the Bureau of Sugar Experiment Stations (BSES).
Concern from scientists at the time saw a temporary ban on the release of the toad, but that was overturned after lobbying of the state government by Queensland cane growers and the BSES.
"It really irks me when that's used as an example to show biological control is a bad thing," said Michael Furlong, a biological control researcher from the University of Queensland.
"There was none of the background work done — the cane toads don't actually eat the cane beetle they were introduced to control.
"It was just really shoddy science that was implemented extremely badly."
A better analogy for modern-day biological control, Professor Furlong said, is the near eradication of the prickly pear.
Until the early 1900s, the prickly pear was the most devastating weed in Australia.
The cactus spread over millions of hectares of land in Queensland and New South Wales, with farmers abandoning swathes of land in its wake.
Arsenic failed to halt its advance, and flamethrowers, tanks and returned soldiers were all put forward as potential solutions that failed to materialise.
In the end, the introduction of a small moth — Cactoblastis — along with a few species of cochineal insects that worked in unison with the moth all but eradicated the pest.
By 1932, 7 million hectares of previously abandoned land was opened back up to settlers.
Professor Furlong said unlike the cane toad, hundreds of millions of dollars was spent on researching the prickly pear eradication plan.
He said the process of establishing a suitable biological control today is incredibly rigorous, taking into account the entire ecosystem that the target species exists in.
"You really need to understand the ecology of the system that you're trying to manage.
"And you really need to have a very detailed understanding of the ecology of the pest — which life stages are susceptible to different mortalities and different natural enemies — the whole demographics of the pest is really, really critical."
For its part, the National Carp Control Plan now consists of nine technical reports bringing together scores of national and international studies on the carp herpes virus.
Could the herpes virus wipe out all carp?
The idea is that the virus will become established in the species, and like viruses in people, will go through periodic peaks and troughs.
Research estimates that the average population could be reduced by 40 to 60 per cent over a 10-year period, though that may be higher or lower depending on location.
The virus kills carp most effectively when waters are between 16 and 28 degrees Celsius. When the virus is in extremely high concentration in the water, it can infect fish without their coming into direct contact with one another.
In other words, it's seasonal and density dependent. So similar to COVID isolation, fish in small isolated pockets are likely to persist without infection, and in high concentrations in the right conditions, it may run rampant.
With carp populations made vulnerable by the virus, it may then be possible to implement other measures like carp busting to wipe out some local populations.
It's likely the fish will persist in our waterways, however, albeit in lower numbers.
Could the virus jump species?
This is probably the biggest question that needs to be answered conclusively before the trial can proceed to implementation phase.
Given that there are no native species of the carp's Cyprinidae family in Australia, the risk is diminished.
And there's already been a lot of research internationally, which has so far only found the disease caused by the virus in European carp and carp hybrids.
Research by CSIRO scientists and colleagues in 2016 exposed 13 native fish, as well as rainbow trout, frogs, crustaceans, chickens, reptiles and mice, to the virus.
The animals were exposed to between 100 and 1,000 times the minimum amount of Cyprinid herpesvirus 3 needed to cause disease in the carp, however, none showed any clinical signs of infection.
Viruses hijack host cells, where the viral DNA is transcribed into mRNA and replicated. Importantly, testing didn't find any viral mRNA in the exposed animals, according to Toby Piddocke, a fisheries biologist with the FRDC, who wrote two of the technical papers in the National Carp Control Plan.
"You can detect the virus's genomic DNA, which just essentially means it's present. To find that is not surprising when you've deliberately exposed that individual to usually quite a high concentration of the virus," Dr Piddocke said.
"It's finding that mRNA, which is the signature of viral replication, [that is important]. None of the species did have mRNA in them."
There has also been no cross-species infection recorded in the wild in Europe where the virus was first found.
However, there were some unanswered questions from the CSIRO research.
"There were some results where some of the non-target species, in both control groups that weren't exposed to the virus and treatment groups that were exposed, had unusual levels of mortality," Dr Piddocke said.
There was no evidence that was due to the virus, but nonetheless the causes of it couldn't be adequately explained.
There have also been instances in European experiments where non-target species exposed to the virus in the lab have been able to pass it on to carp.
Again though, this doesn't mean the non-target species is actually infected. It could be an instance of what in hospital settings is called "fomite transmission" or "mechanical vectoring", Dr Piddocke said.
"The equivalent in the hospital would be like a towel that has the virus or something on it and somehow gets passed between patients or ... something like flu virus on a lift button."
Overall, there hasn't been any solid evidence that non-carp species can become infected with the virus.
Nevertheless, the National Carp Control Program is recommending more research be done in this area before the program proceeds.
"Because it is such a crucial consideration for a bio-control agent, we have lent on the side of caution there, and therefore recommended more work in that area," Dr Piddocke said.
And even if a virus can be transmitted in a laboratory setting, which is sometimes done via direct injection, Professor Furlong said that doesn't mean it will necessarily be a problem in the wild.
"Often with pathogens for example, organisms ... can actually contract the disease [in a laboratory], but whether they do in nature depends on a lot of other things.
"[For example] they don't come into contact with [the pathogen] at the right life stage or it can't penetrate and actually infect them."
What's next?
So where does all this leave the plan?
At this point it's still under national consideration. Meaning, it's still on the cards, but there is more work to be done, according to Hayden Ferguson — a principal policy officer in pest fish with Biosecurity Queensland.
"The efficacy of the virus, the safety of the virus, and potential ecological impacts that may be associated with the release of the virus are undergoing further consideration," Mr Ferguson said.
And in terms of how long it may be until we have an answer one way or another?
"There's currently no timeline in terms of the release of the virus because of these numerous considerations and uncertainties that have been raised and the resolutions that need to be sought [in order to] address them," Mr Ferguson said.
So will Mr Joyce's dream come true? Will we see "a version of venereal disease" used to help restore "the environmental health of our rivers and waterways" for the benefit of "silver perch, the yellow-belly, the Murray cod, the eastern cod and the catfish"?
More research will clearly be needed to be absolutely sure that only the right species get herpes.
