Imagine coasting through flu season with barely a sniffle. Or brushing off COVID, no matter how many times it mutated.
Imagine, in fact, that no virus can harm you, from chickenpox to Dengue to HIV. Even the deadliest viruses we know of, like rabies or Ebola, don't cause you serious problems.
For a handful of people, this seems to be the case. Anyone with a specific and rare genetic mutation benefits from a superpowered side-effect: they fight off viruses with ease, to the extent that most of the time, they don’t even know they’ve been infected.
The mutation in question causes a deficiency in a key immune system protein called ISG15. In turn, this leads to a mildly elevated systemic inflammation in their bodies – it’s this inflammation that seems to subdue any virus that tries to get past.
When Dusan Bogunovic, professor of immunogenetics at Columbia University in New York, first discovered the mutation 15 years ago, he didn’t realise what was in front of him.
“I don’t know that ‘ignorant’ is the right word, but I was unaware of this possibility for the first three years after we discovered it,” he says. “I wasn’t studying viruses.”
It was only when he took a job at a lab that was studying viruses that it dawned on him. He remembers going to seminars to learn more.
“That was the ‘Eureka moment’,” he recalls. “That was when I suddenly thought: ‘Wait, the autoinflammation profile in these rare patients is 100-per-cent antiviral!’”
Sure enough, when he went back from the seminars and studied the ISG15 patients’ immune cells, Bogunovic found they had encountered several viruses during their lives, including flu, measles, mumps and chickenpox.
Only these patients had never shown any of the symptoms associated with them.
Their immune systems, in a permanent state of high alert due to their genetic mutation, had never allowed the viruses any kind of foothold.
“Think about when someone in your household gets the flu,” Bogunovic says. “They’re floored by it, but the person they share a bed with only gets a little bit of sniffles and a sore throat. In a way, you can think of this mutation like those people who just go through the sniffle phase.
“What’s even cooler is, it’s your own DNA that makes you ready when the virus comes. The machinery that’s evolved to fight off viral infections is just slightly enhanced.”
The discovery gave Bogunovic an idea. A big one.
What if we could create a drug that mimics the effect of the mutation? And what if you could control the inflammation response so that your levels aren’t chronically elevated, like people with the mutation? You just switch it on when you need it – when there’s a virus.
The possibilities for such a drug didn’t end there, however. What if it didn’t treat just one virus, but entire viral families? In fact, what if you could make a universal antiviral that was effective against every virus we know of, and even the ones we don’t?
Such a drug would be world-changing – a medical multitool unlike anything we’ve seen before in the treatment of viral infections.
It wouldn’t just mean we all feel better in the winter. This kind of breakthrough would save countless lives and massively lower the burden on public health systems worldwide.
Then, if another pandemic-level virus, like COVID, emerged tomorrow, we’d have a treatment on the shelf that could stop it in its tracks.
Miracle medicine, but real
A single drug that’s effective against every sort of virus sounds like a researcher’s idle daydream, the ultimate medical what-if. The thing is, Bogunovic and his colleagues may have already achieved it, or at least something close.
In summer 2025, they published results of an experiment in which mice and hamsters were given a drug inspired by people with ISG15 deficiency.
It’s a cocktail of 10 gene products, all of which are elevated in people with the mutation. Researchers exposed the animals to influenza and SARS-CoV-2, the virus that causes COVID. Neither virus was able to replicate in the animals, nor cause them severe symptoms.
“This was the first time in vivo – in living animals – showing that this drug can work,” Bogunovic says. “Of course, prior to that, we tested it against 10 different classes of viruses in vitro and couldn’t find one against which it didn’t work.”
In other words, in cell cultures in the lab, no virus has been able to break through the treatment’s defences.
Broad-spectrum antivirals – drugs that treat multiple viruses – are not a new idea. Remdesivir, for example, is an antiviral used to treat COVID, but it was originally developed for hepatitis C and has also been tested for Ebola, albeit with limited results.
Research into broad-spectrum antivirals has intensified over the last 15 years in response to multiple viral threats such as Middle East respiratory syndrome (MERS), Zika virus, Ebola and monkeypox.
And that’s to say nothing of COVID, the biggest health crisis in a century, which unsurprisingly renewed interest and fast-tracked research money (including a large effort to repurpose existing drugs for the new viral threat).
But broad-spectrum antivirals are difficult to develop, mostly because drugs that treat viruses usually target proteins on a virus’s surface.
For a drug to work on multiple pathogens, the target protein would need to be the same from virus to virus. This is rarely the case, even in closely related viruses.
There are drugs that work for SARSCoV-1, for example, which don’t work for SARS-CoV-2.
Even so, it seems that research is now paying off because Bogunovic’s team is not the only one to report impressive results. In 2025 alone, multiple groups have published research on broad-spectrum antivirals.
Sugarcoated antiviral medicine
One particularly promising and novel option comes from a team of researchers led by Prof Adam Braunschweig at the City University of New York and Prof Hector Aguilar at UCLA.
Together, they have created a drug that targets sugars on the surface of a virus rather than its proteins. While proteins are different from one virus to the next, sugars are largely the same.
“That’s because it turns out viruses don’t make sugars,” says Braunschweig. “They steal them from the host. So in fact, most of the COVID circling around in your body is covered with sugars that it stole from you.
“And if these sugars are made of you, your body doesn’t know that they’re bad. That’s how the virus can enter the cell.”
The team’s new therapy binds to these same sugars. It stops viruses from evading the host’s immune system and invading the cells.
In lab tests, Braunschweig and his colleagues have tested their drugs against multiple viruses, representing five viral families. In a smaller study in mice, a single treatment protected 90 per cent of animals against COVID.
“It’s effective against 100 per cent of the viruses we’ve tested it against,” Braunschweig says. “These include influenza viruses A and B, bird flu and filoviruses, like Ebola and Marburg.”
Braunschweig and his colleagues are already planning human trials, currently scheduled to begin in two years. Meanwhile, other researchers continue to explore different ways of developing broad-spectrum antivirals.
A team in Germany found that a drug that treats diabetes could also cut the viral load of viruses like SARS-CoV-2 and Dengue. Other researchers, forming a global non-profit collective called the COVID Moonshot, have developed an open-science broad-spectrum drug candidate for coronaviruses.
Protease inhibitors are yet another option, with drugs targeting enzymes that viruses need to make copies of themselves.
The race is very much on to find a universal antiviral, but there are also voices urging caution when it comes to the research, including scientists who have already made broad-spectrum drugs.
“I’m sort of a poster child for this,” says Prof Raymond Schinazi, a virologist at Emory University in Atlanta, Georgia, “because I discovered drugs for HIV that also work against hepatitis B.”
He thought it was quite the breakthrough until he realised the potential for both viruses to mutate and develop a resistance to those drugs. Or the other alternative: that by treating one condition, you get resistance to the other.
“Then you’re in trouble,” he says, “real trouble.”
Schinazi says two camps are emerging among scientists: those who are excited about the potential of broad-spectrum drugs and those who prefer very specific compounds. He belongs to the latter.
“We are very keen, in my lab, on finding a specific antiviral agent. One virus, one antiviral,” he says.
His point is not that silver bullet antivirals won’t work, it’s that we need back-ups: multiple drugs that work in multiple ways, combined with vaccines, to give several layers of protection against a given virus.
“It’s a bit like driving a car,” Schinazi says. “You need the seatbelt and you need the airbag. Same thing with viruses. If you have vaccines available, as well as drugs, you’re beautifully set up in case a virus blows up. You’re ready to annihilate that virus.”
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These drugs could have unintended consequences
There are other challenges facing the researchers who are developing these treatments. One is the risk that a compound is so wide-acting that it does something you don’t want it to do. “We are always worried about side effects and off-target effects,” says Schinazi.
It’s something Braunschweig is keenly aware of in his research. The type of sugar his team is targeting doesn’t just appear on the surface of viruses; it appears on every human cell. “We’re targeting something that we obviously need,” he says.
So how do you make sure the drug you’re making isn’t toxic to the people you’re trying to protect?
“Well, all drugs have toxicity at certain concentrations,” Braunschweig says, from cancer drugs to paracetamol. “I think Tylenol [paracetamol] has probably the most unintended overdoses for an over-the-counter drug because people take huge dosages.
“The question is whether you can find a therapeutic dose for your drug that’s far from the toxic dose. It’s whether you can target something with an acceptable therapeutic window. For me, the upside is so big that it was worth trying.”
The compound Braunschweig and his colleagues have developed seems to have a very broad window. In other words, at this preclinical stage, it’s safe.
“We see some toxicity at 100 milligrams per kilogram, [mg/kg]” he says. “But the therapeutic dose that we tested was 2mg/kg. We also tested 10mg/kg and observed no toxicity whatsoever.”
The next challenges for researchers are practical, logistical and financial. Braunschweig and Bogunovic are both looking ahead to human trials. But first, there’s a molecular engineering job to be done to ensure the drugs are packaged and delivered in a way that works safely.
“That technology is improving, but it’s not perfect yet,” Bogunovic says. “Then you have the fact that this is a new class of drugs against infections.
“So you need partners in regulatory bodies who understand and want to advance this in the most ethical, standardised, appropriate way. And then, of course, somebody has to finance it.”
Money could be a serious barrier. For all the research grants awarded after the COVID pandemic, clinical trials are still notoriously expensive.
“From drug optimisation to phase one [the first time a new drug is tested in humans], and then phase one through to a drug that’s approved by regulators, we’re probably talking about a billion dollars,” Bogunovic says.
“And how do you run a clinical trial for a universal antiviral? You have to run it virus by virus, which makes it extremely expensive.”
For biotech companies that need a return on their investments, it’s high-risk, especially when it comes to preparing for the next pandemic. Because in that scenario, you’re effectively developing drugs that we all hope we never need.
“If I told you, the investor, there’s going to be SARS-CoV-3 in two years, but we can get a drug to the market in time,” Bogunovic says, “that’s great. We help people, people won’t die and we make a profit.
“But I can’t tell you what will happen. In fact, I hope it doesn’t happen.”
So how do you convince investors to fund the drug anyway? Bogunovic believes we need public-private partnerships, where governments fund and stockpile broad-spectrum drugs.
If we’d done that before 2020, the COVID pandemic would have looked very different, he says.
“It’s hard to say for a fact, but if we’d had these drugs in 2020, I do think we would have saved lives, we would have saved the economy, and we would have saved mental health and education.”
Preparing for another pandemic
The threat of another viral pandemic has hardly gone away. Governments and researchers alike have repeatedly stated the need to learn the lessons from COVID.
But when life returns to normal, and when everything from wars to public services to climate change is competing for public money, it’s easy to collectively forget that viruses are one of the biggest threats to humanity’s continued survival.
That’s what makes a universal antiviral so appealing. A drug with far-reaching effects could lessen the burden of viruses that exist today and – hopefully – work for the next one that emerges.
In the pandemic scenario, Braunschweig says the biggest impact would be to prevent the infected from becoming patients and save health services from being overwhelmed like they were in 2020.
“Let’s say this stuff works like broad-spectrum antibiotics. You may still suffer, but it lowers the intensity of the disease. Then only the most severe cases need those hospital beds.”
And in the meantime, these new drugs could give us the upper hand in the perennial fight against viruses.
“It’s hard to overstate the potential impact,” Braunschweig says. “We can imagine a molecule that costs a dollar a dose and works against every virus with at least some impact.
“The spectrum could be from HIV to the common cold, to Nipah and Hendra. In other words, it could eliminate as a threat our greatest enemy throughout the history of our species.”
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