Curing disease is really a matter of outfoxing evolution. When we assault bacteria or viruses or cancer cells with drugs, they evolve ways of resisting those drugs. We attack, they counter-attack. Take malaria: the Plasmodium parasites that cause the disease have repeatedly evolved to resist our best anti-malarial drugs. The mosquitoes that carry the parasites have evolved to resist the insecticides we poison them with. And now, Victoria Barclay from Pennsylvania State University has found that some malaria vaccines could drive Plasmodium to become even deadlier than it is now.
Several malaria vaccines are in development, but none have been licensed yet. Barclay vaccinated mice with a protein that’s found in several of these vaccines, and then exposed them to Plasmodium. After a few generations, the parasite became more ‘virulent’ – that is, it caused more severe disease. And it did so via an evolutionary escape route that is rarely considered.
HIV is an exceptional adversary. It is more diverse than any other virus, and it attacks the very immune cells that are meant to destroy it. If that wasn’t bad enough, it also has a stealth mode. The virus can smuggle its genes into those of long-lived white blood cells, and lie dormant for years. This “latent” form doesn’t cause disease, but it’s also invisible to the immune system and to anti-HIV drugs. This viral reservoir turns HIV infection into a life sentence.
When the virus awakens, it can trigger new bouts of infection – a risk that forces HIV patients to stay on treatments for life. It’s clear that if we’re going to cure HIV for good, we need some way of rousing these dormant viruses from their rest and eliminating them.
A team of US scientists led by David Margolis has found that vorinostat – a drug used to treat lymphoma – can do exactly that. It shocks HIV out of hiding. While other chemicals have disrupted dormant HIV within cells in a dish, this is the first time that any substance has done the same thing in actual people.
At this stage, Margolis’s study just proves the concept – it shows that disrupting HIV’s dormancy is possible, but not what happens afterwards. The idea is that the awakened viruses would either kill the cell, or alert the immune system to do the job. Drugs could then stop the fresh viruses from infecting healthy cells. If all the hidden viruses could be activated, it should be possible to completely drain the reservoir. For now, that’s still a very big if, but Margolis’s study is a step in the right direction.
HIV enters its dormant state by convincing our cells to hide its genes. It recruits an enzyme called histone deacetylase (HDAC), which ensures that its genes are tightly wrapped and cannot be activated. Vorinostat, however, is an HDAC inhibitor – it stops the enzyme from doing its job, and opens up the genes that it hides.
It had already proven its worth against HIV in the lab. Back in 2009, three groups of scientists (including Margolis’ team) showed that vorinostat could shock HIV out of cultured cells, producing detectable levels of viruses when they weren’t any before.
To see if the drug could do the same for patients, the team extracted white blood cells from 16 people with HIV, purified the “resting CD4 T-cells” that the virus hides in, and exposed them to vorinostat. Eleven of the patients showed higher levels of HIV RNA (the DNA-like molecule that encodes HIV’s genes) – a sign that the virus had woken up.
Eight of these patients agreed to take part in the next phase. Margolis gave them a low 200 milligram dose of vorinostat to check that they could tolerate it, followed by a higher 400 milligram dose a few weeks later. Within just six hours, he found that the level of viral RNA in their T-cells had gone up by almost 5 times.
These results are enough to raise a smile, if not an outright cheer. We still don’t know how extensively vorinostat can smoke HIV out of hiding, or what happens to the infected cells once this happens. At the doses used in the study, the amount of RNA might have gone up, but the number of actual viral particles in the patients’ blood did not. It’s unlikely that the drug made much of a dent on the reservoir of hidden viruses, so what dose should we use, and over what time?
Vorinostat’s actions were also very varied. It did nothing for 5 of the original 16 patients. For the 8 who actually got the drug, some produced 10 times as much viral RNA, while others had just 1.5 times more. And as you might expect, vorinostat comes with a host of side effects, and there are concerns that it could damage DNA. This study could be a jumping point for creating safer versions of the drug that are specifically designed to awaken latent HIV, but even then, you would still be trying to use potentially toxic drugs to cure a long-term disease that isn’t currently showing its face. The ethics of doing that aren’t clear.
Steven Deeks, an AIDS researcher from the University of California San Francisco, talks about these problems and more in an editorial that accompanies the new paper. But he also says that the importance of the study “cannot be overstated, as it provides a rationale for an entirely new approach to the management of HIV infection”.
Reference: Archin, Liberty, Kashuba, Choudhary, Kuruc, Crooks, Parker, Anderson, Kearney, Strain, Richman, Hudgens, Bosch, Coffin, Eron, Hazudas & Margolis. 2012. Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy. Nature http://dx.doi.org/10.1038/nature11286
Image by Dr. A. Harrison; Dr. P. Feorino
More on HIV:
A malarial mosquito is a flying factory for Plasmodium – a parasite that fills its guts, and storms the blood of every person it bites. By hosting and spreading these parasites, mosquitoes kill 1.2 million people every year.
But Plasmodium isn’t the only thing living inside a mosquito’s guts. Just as our bowels are home to trillions of bacteria, mosquitoes also carry their own microscopic menageries. Now, Sibao Wang from Johns Hopkins Bloomberg School of Public Health has transformed one of these bacterial associates into the latest recruit in our war against malaria. By loading it with genes that destroy malarial parasites, Wang has turned the friend of our enemy into our friend.
Many groups of scientists have tried to beat malaria by genetically modifying the species of mosquito that carries it – Anopheles gambiae. Marcelo Jacobs-Lorena, who led Wang’s new study, has been at the forefront of these efforts. In 2002, his team loaded mosquitoes with a modified gene so that their guts produce a substance that kills off Plasmodium.
When Rachel Carson wrote her famous book Silent Spring, she envisioned a world in which chemical pollutants killed off wildlife, to the extent that singing birds could no longer be heard. Pesticides aside, we now know that humans have challenged birds with another type of pollution, which also threatens to silence their beautiful songs – noise.
A man-made world is a loud one. Between the din of cities and the commotion of traffic, we flood our surroundings with a chronic barrage of sound. This is bad news for songbirds. We know that human noise is a problem for them because some species go to great lengths to make themselves heard, from changing their pitch (great tits) to singing at odd hours (robins) to just belting their notes out (nightingales). We also know that some birds produce fewer chicks in areas affected by traffic noise.
Now, Julia Schroeder from the University of Sheffield has found one reason for this. She has shown that loud noises mask the communication between house sparrow mothers and their chicks, including the calls that the youngsters use to beg for food. Surrounded by sound, the chicks eat poorly. “City noise has the potential to turn sparrow females into bad mothers,” says Schroeder.
Here is an unfortunate clash of circumstance. Vaccines and antibiotics become useless in heat, but the countries where they are most needed – poor ones where infectious diseases are a major cause of death – are really hot. Because of this, millions of dollars are spent on keeping vaccines cold and millions of lives are affected when they can’t be.
The factory that makes a vaccine can be continents away from the arm of the child who will receive it. Those distant points are separated by the “cold chain” – a network of refrigerators, freezers, insulated vehicles, cold boxes, specially equipped depots, and trained personnel. If the chain fails, and vaccines are allowed to heat up, they rapidly and permanently degrade. This happens even in developed countries, but it’s a huge problem for developing ones, where electricity and refrigeration can be sparse luxuries.
If there was a way of stabilising vaccines so they can withstand high temperatures, it could save millions of both lives and dollars. And Jeney Zhang, a graduate student from Tufts University, has developed one possible method: wrapping vaccines and antibiotics in molecular cages of silk.
Within these prisons, the MMR vaccine and two common antibiotics were still viable after months at high temperature. Matt Cottingham, a vaccine specialist from the University of Oxford, says, “The stability is amazing. No one’s even come close to that. It’s certainly better than anything else that’s currently being used.”
Silk is no stranger to medical applications. Spewed from the salivary glands of silkworm caterpillars, this natural fibre is strong, flexible and biodegradable. It has been used to make surgical sutures, medical implants, and replacement tissues. It can also be used to imprison small molecules. Individual silk molecules come together to form a structure with tightly organised regions, interspersed with looser “pockets”. In these pockets, molecules can be shielded from the elements.
Zhang, working in the lab of silk maestro David Kaplan, showed that silk can stabilise two antibiotics – penicillin and tetracycline – as well as the measles, mumps and rubella (MMR) vaccine.
Wrapped in silk, penicillin spent a month at 60 degrees Celsius with no loss of activity. Normally, it breaks down after a few weeks at room temperature (25C), or just a day at human body temperature (37C) – a month at 60 is unheard of. Tetracycline is even more delicate. In silk, it lost 20 per cent of its activity after a month at 60C, and was unharmed at lower temperatures.
The MMR vaccine fared similarly well. The vaccine consists of weakened versions of the viruses behind the three diseases. They are shipped as a freeze-dried powder, which has to be dissolved in a special solvent before being injected.
If the powders are kept at 45C, they become completely useless within 20 weeks. If the viruses are wrapped in silk before being freeze-dried, they stay almost good as new, keeping at least 85 per cent of their original potency after 6 months, no matter the temperature. Put it another way: at 37C, it would normally take 9 weeks for the viruses to lose half their original potency, but it takes 94 weeks if they are encased in silk.
How does the silk protect its payload? It’s not clear. The silk may protect the viruses in the vaccines from enzymes that would otherwise destroy the proteins on their outer shells. Without those proteins, the immune system has no way of recognising what the virus looks like, or preparing itself for future infections. The silk might also act as a physical barrier that constrains the viral proteins and stops them from deforming at warmer temperatures. And it could keep water away from the vaccines.
There’s clearly still a lot of basic questions left to answer, not least, as Cottingham asks: “Would this be compatible with being injected into babies?” Kaplan expects so. “Silk has been used in medical devices, such as sutures, for decades and the FDA approved it for new medical products more recently,” he says. It’s a promising first step towards making the cold chain a little less brittle.
Reference: Zhang, Pritchard, Hu, Valentin, Panilatitis, Omenetto & Kaplan. 2012. Stabilization of vaccines and antibiotics in silk and eliminating the cold chain. PNAS http://dx.doi.org/10.1073/pnas.1206210109
Image by GiveWell
Any study that claims to overturn long-held dogmas is going to run headlong into controversy. Take, for example, a stream of recent papers which apparently showed that adult ovaries contain stem cells capable of producing eggs.
If that’s true, it’s a really big deal. For decades, the textbooks have said that women are born with their lifetime supply of eggs, which slowly dwindle away and are never replaced. If adult ovaries do indeed have stem cells that can regenerate new eggs, that has big implications for fertility treatments, and when a woman could potentially have children.
But wait! A new study, which used a different technique to isolate these ovarian stem cells in mice, found that they don’t divide, and never produce actual eggs. Maybe the textbooks are fine as they are?
But WAIT! This study, far more than many of the others I cover, has divided opinion. Obviously, the authors think that it deals a critical blow to the idea of egg-making adult stem cells. And obviously, one of the people behind the stem cell discovery thinks that the new experiments aren’t very good. I also contacted four other scientists who work on ovarian biology and their views differ considerably.
I’ve written about this story for The Scientist so head over there for the details, and the grounds for the disagreement.
Image from RWJMS IVF Laboratory
A migrating robin can keep a straight course even when it flies through a cloudy night sky, devoid of obvious landmarks. That’s because it can sense the Earth’s magnetic field. Something in its body acts as a living compass, giving it a sense of direction and position.
This ability – known as magnetoreception – isn’t unique to robins. It’s been found in many other birds, sharks and rays, salmon and trout, turtles, bats, ants and bees, and possibly cows, deer and foxes. But despite more than 50 years of research, the details of the magnetic sense are still elusive.
Unlike light, sounds or tastes, which come and go, the Earth’s magnetic field is always ‘on’. To study how animals sense it, scientists first have to cancel it out using magnetic coils, and set up their own artificial field. The field also pervades the entire body, so there’s no obvious opening, like an eye socket or ear canal, where a magnetic sensor would most likely lie.
In birds – the best-studied of the magnetic-sensing animals – scientists have narrowed down the location of a possible sensor to the eye (sometimes, just the right one), the beak, and possibly the inner ear. But it’s been far trickier to find the individual cells responsible for sensing magnetic fields. Now, Stephan Eder from the Ludwig-Maximilians-University in Munich has developed a way of doing that. It’s deceptively simple: look at cells under a microscope surrounded by a rotating magnetic field, and spot the ones that start to spin.
Flesh-eating plants are basically nitrogen thieves. The speed of their growth is limited by this invaluable element, just like all other plants. The difference is that plants that eat animals, like pitcher plants and the Venus fly trap, grow in places like swamps and rocky outcrops, where nitrogen in thin on the ground… or thin in the ground. They have to supplement their supply by stealing nitrogen from the bodies of animals. This is why some plants become killers.
Let me clarify that: this is why some plants become obvious killers. Scott Behie from Brock University has found that a far greater range of plants can inconspicuously assassinate animals by proxy. They partner up with an infectious fungus that kills insects and transfers their precious nitrogen to the plant. Thanks to the fungi, the plants become indirect predators.
Australians love to destroy cane toads. Ever since these animals were first introduced in 1935, they have run amok, eating local animals and poisoning any that try to eat them. They’re captured and slaughtered in traps, bludgeoned with golf clubs, and squished with veering tyres, but still they continue to spread. Now, Michael Crossland from the University of Sydney has discovered an unlikely ally in the quest to control the cane toad: the cane toad.
Along with their unappealing appearance and milky poison, cane toads are also cannibals. Older tadpoles will hunt and eat eggs that have been recently laid in the same pond, to do away with future competitors. Crossland reasoned that the eggs must release a substance that the tadpoles can detect, so he mushed them up in his lab and separated out their chemical components.
He discovered that the eggs secrete bufadienolides – the same substances that make the milky poisons of the adult toads so deadly to Australia’s fauna. Ironically, the same chemicals that protect the eggs later in life also attract cannibalistic tadpoles. And that makes them excellent bait.
When we think about preparing for pandemics, we think about vaccines, stockpiles of drugs, and surveillance. We rarely think about research. This oversight means that when big epidemics hit, like the swine flu pandemic of 2009, scientists lose valuable chances to find more about these illnesses. A new consortium is out to change that. I wrote about their work, and the problem of slow clinical research in a new feature for the BMJ, which I’m reprinting here.
While viruses are fast and adaptable, clinical research is lumbering and cumbersome. Epidemics tend to arrive with little warning, spread quickly, and end abruptly. By contrast, clinical trials can take months to plan. Forms must be designed to record the right data and ethical approval must be sought. By the time would-be researchers can vault over these obstacles the epidemic is history.
This explains why, during the 2009 A/H1N1 influenza pandemic, virtually no patients were enrolled in a randomised controlled trial designed to identify the best ways of treating the infection. Such trials are the gold standard of medicine and the best way of getting rigorous evidence for a treatment’s effectiveness. During the pandemic millions of people were treated with the front line drug oseltamivir (Tamiflu). But the only evidence that oseltamivir actually saved lives came from retrospective observational studies, with all the biases they entail. To this date, serious questions remain about the drug’s effectiveness. “A Tamiflu trial during the last pandemic would have resolved all the controversy over whether it works or not,” says Mike Clarke, Director of the UK Cochrane Centre. In the UK people could request doses of the drug through an NHS hotline. “On the first day of that system, 5000 people received Tamiflu. On that day alone, you could have conducted the biggest trial in the world ever,” says Carl Heneghan from the University of Oxford.Tamiflu’s relatives, zanamivir and peramivir, are similarly mysterious. Are they actually effective against the pandemic strain? What are their ideal doses? Should a high loading dose be used at the start of treatment? Can they be used in combination? Are they suitable for the groups who seem to experience the most severe infections, such as obese people, pregnant women, infants, or those with other diseases? We do not know the answers to these questions, and our ignorance is all the more galling because the virus infected between 11 and 21% of the world’s population.
The same questions dog the many other treatments that doctors turned to during the pandemic, such as steroid hormones, immunoglobulin antibodies, and transfusions of plasma from patients who had fought off the virus. Several thousand patients had such severe problems with their hearts and lungs that doctors had to divert their blood out of their bodies and perfuse it with oxygen by machine—a last ditch treatment known as extracorporeal membrane oxygenation. Each measure has at least one report claiming that it is effective, but these reports are always based on small non-randomised studies. Randomised controlled trials were nowhere to be seen.
“Disgrace is too strong a word, but it’s a shame that we don’t know the answers to these questions after this disease has been through not just poor countries but ours,” says Jeremy Farrar, professor of tropical medicine at Oxford University, who studies infectious diseases in Vietnam. “So much of the world’s population saw this virus.”
These problems are not restricted to pandemic flu: the same barriers have held back our knowledge of other infections. If severe acute respiratory syndrome (SARS) sprang up today, doctors would still ask questions about whether to give patients steroids, immunoglobulins, or ribavirin. And with the sluggish speed of clinical research, they would neither have the answers, nor be in a position to get them. “Let’s say they announce cases of SARS in Vietnam today,” says Piero Olliaro from the World Health Organization, “can we start doing a study? No. Our response is very poor.”
“We don’t ever make the progress we should,” says Farrar. “If a patient comes in tonight with Nipah virus, we can’t look at research done five years ago and say, ‘Look, we should treat this individual in this way.’ Those people would be subject to all sorts of bizarre treatments and we don’t know if they’d work or not.”
Some scientists have had enough. Farrar and others have joined forces to create a global alliance called the International Severe Acute Respiratory Infection Consortium (ISARIC), which will ensure that scientists can carry out effective clinical research during future epidemics. Formally announced in December 2011, ISARIC already includes between 50 and 60 research networks across six continents, and it is still growing. Its supporters include a who’s who of big medical funding agencies: the Wellcome Trust, the UK Medical Research Council, the Bill and Melinda Gates Foundation, Institut National de la Santé et de la Recherche Médicale (Inserm), the Li Ka Shing–University of Oxford Global Health Programme, and the Singapore Ministry of Health.
ISARIC’s goal is to set up relationships, protocols, and strategies during this peacetime period, so that researchers can hit the ground running when the next major infection emerges. When people talk about preparing for epidemics they usually refer to monitoring potential threats or stockpiling drugs and vaccines. ISARIC will deal with the crucial missing element: it will prepare to study epidemics as they happen. Everything from personnel to ethical approval will be readied beforehand, so that when the time comes research can progress at the pace of the virus.
Perhaps the most striking aspect of ISARIC is that it is only now being set up. The last pandemic was preceded by decades of concern about flu, but the preparation focused on epidemiology, modelling, and public health approaches. There was plenty of time to prepare ready made trials, but none was set up. Heneghan thinks that this complacency was partly driven by an inflated sense of certainty about treatments, despite a weak evidence base. “Some people still think we should just use existing treatments when we have influenza, and that’s just what we do,” he says.
“Some people just don’t think into the future enough,” says Clarke. “It’s very surprising that we haven’t got off the shelf trials for major incidents that you know are going to happen.” Farrar adds, “I think nobody thought of [doing this]. If they did, they probably concluded that funding agencies would not fund something that was designed for an uncommon event that would occur at [an] unpredictable time in the future.”
If such reticence once existed this is now changing. In the UK, the National Institute for Health Research (NIHR) put out a call for research proposals in the spring of 2009, as the pandemic was emerging. Despite a fast turnaround, those studies only started after the main waves of infection had passed. Fast was not fast enough. So in October 2011 the NIHR agreed to fund eight projects, including several clinical studies, which will be activated if another pandemic reaches the UK. Steve Goodacre from the University of Sheffield, who chaired the meeting that funded these proposals , says, “You’d get ethics and regulatory approval, pilot the project, develop data collection forms, set up everything ready to go, and put it on hold until a pandemic happened.” At that point full funding would be released, and the pre-cocked starting pistol would fire. Clarke is involved with one of the funded trials, which will assess the use of low dose steroids as treatments for pandemic flu. “It’s ready to go when someone says start,” he says. “The UK may be ahead of the game here.”
ISARIC, which is collaborating with many of the investigators funded by the NIHR, will extend the same principles worldwide. Its first seeds were planted in November 2010, three months after the H1N1 pandemic had officially come to an end. In its aftermath several biomedical funding organisations, including the Bill and Melinda Gates Foundation, the Wellcome Trust, Institut Pasteur, and the National Institute of Allergy and Infectious Diseases, gathered in Bethesda, Maryland to discuss gaps in research on influenza and other respiratory diseases. The problem of slow research response stood out.
The Wellcome Trust followed up with a meeting to discuss the problem in February 2011. Representatives from 20 clinical networks gathered in London, along with funding agencies, and public health workers from WHO, the US Centers for Disease Control and Prevention (CDC), and more. They all recognised the same problem and agreed to work together to solve it. “There was a dramatic, enthusiastic endorsement,” recalls Fred Hayden from the Wellcome Trust. “There was a lot of commitment even then.” ISARIC was born.
The consortium has since grown in size, and there are currently no restrictions as to the number of networks that can join. ISARIC has won two years of funding, amounting to around £500<thin>000, to set their ambitious plans in motion. But, despite the enthusiasm around the consortium, its members recognise that speeding up the pace of clinical research is a significant challenge.
Even the simple business of recording a patient’s details becomes tricky. You need to decide how to diagnose someone as a case so that you end up with the right sample. You need to work out the criteria on which to include or exclude a patient from a trial. You must decide what research questions to ask so that you know what information to record. Creating these case record forms already takes a lot of time, and there’s more still to be done.
Once a research plan has been nailed down it can take months to get funding and ethical approval, at a time when responses are needed in hours and days. For example, in one review of cancer trials it took an average of 621 days to recruit the first patient after funding had been agreed. The recent H1N1 pandemic came and went in less time. “That might be okay for hypertension or diabetes in a developing country, but for a rapidly developing problem, we have to concertina that,” says Farrar.
In ISARIC’s vision clinicians would develop these research protocols ahead of time and secure ethical and administrative approval. When a crisis hits, these plans could be fed through a fast tracked system that allows research to start immediately. Farrar likens this system to the rapid response approaches already used by public health authorities. “If there was an outbreak of salmonella in America tomorrow, there’ll be a really good, well-organised response from the CDC,” he says. “They won’t spend six months discussing a protocol and putting together a case record form. They go to a shelf and take off how they investigated it the last time.”
Researchers also need to work from the same playbook, even if they hail from different regions or countries. If everyone records the same data then local information becomes globally useful. “In an outbreak, you may only be able to study 20 patients in Vietnam, 30 patients in China, and 30 in Africa,” says Farrar. “We need to make sure that we standardise these things so that ultimately, we can bring all of that research together.” As the infections spread data would accumulate.
To ISARIC’s researchers, it is crucial that such data be stored in a freely available repository. The open access movement has been very successful in promoting free access to the end results of research, such as data and publications. But Farrar says that the same principles should apply to the materials that make research possible in the first place. “If you faced an outbreak of encephalitis in Outer Mongolia, you could go to an open access website and say, ‘This group in Vietnam have done lots of studies on encephalitis, and here are their case record form, inclusion criteria, and consent sheet.’ That might save you months of effort.”
People also have to be ready for the chaos that epidemics sow. “Things become significantly more difficult,” says Olliaro. “There’s disruption, panic, and a lot of media attention.” Clinics are flooded with patients, and clinicians face extra burdens on top of their already busy schedules. They barely have time to do regular work, much less carry out additional research. As the epidemic continues clinicians could fall ill themselves, compounding any shortness of staff. If clinics are to cope they need specialists who are trained to carry out research in the event of an epidemic. “You need an intervention squad,” says Olliaro. “They’re ready to go but don’t know when they’ll be called upon. In the mean time, they’re doing routine hospital work.”
Such systems would be impossible to create in the middle of a crisis: they need to be put in place in the breathing space between epidemics. For ISARIC, this does not mean just making plans and forms, but creating trust and connections between its international members. Hayden recalls that during the London meeting when the idea for a consortium was first mooted, “a lot of these groups didn’t even know what each other were doing.” Farrar says, “Ultimately, what drives science is still relationships. The time to build trust is now, outside of the pandemic setting. Then, when you have a crisis, you can be on the phone to someone in Indonesia and they trust you because you’ve worked together and you didn’t steal their samples.”
With their initial burst of funding, the ISARIC members have set up a secretariat and four working groups to advance their agenda. The first working group is tasked with designing clinical trials that can begin now, but that can also adapt and continue in the event of an epidemic. The second group will collect and standardise the clinical data we already have on H1N1 and other emerging infections. The third will develop protocols for studying the basic biology of infections with epidemic potential, such as how they affect their hosts, what makes some people more susceptible than others, and how they might react to known drugs. The fourth group will map all the barriers to a rapid clinical response, and create an open access hub that is loaded with pre-approved plans and documents to be deployed in a crisis.
Within the next two years, ISARIC hopes to build up enough momentum to secure more funds for the research they devise and to sustain the collaboration in the years ahead. Their ambitions are large, but Steven Webb from the Royal Perth Hospital, Australia thinks that they need to move quickly. “There’s a window of opportunity for funding,” he says. “People tend to remember the last great threat to public health and, at the moment, attention has been drawn to infectious diseases because of the last pandemic. We look to capitalise on that window of opportunity before it closes.”
Image by Eneas de Troya