Most antiviral drugs are designed to target one specific virus, such as the flu or HIV.
But what if there were a way to create a medicine that could fight off many different viruses at once?
A team of scientists from MIT and several partner institutions may be moving closer to that goal.
In a study published in Cell, researchers report the discovery of compounds that help human cells activate their own built-in defense system against viral infections.
These compounds work by turning on a process called the integrated stress response pathway. Normally, this pathway is triggered when a virus begins to replicate inside a cell.
It works by shutting down protein production so the virus can no longer make the proteins it needs to spread.
By boosting this natural defense, the compounds may be able to stop a wide range of viruses in their tracks.
The research team screened nearly 400,000 chemical compounds to find ones that could amplify this stress response. Using a novel approach called optogenetics, they engineered cells so that the stress pathway could be switched on by blue light.
When they exposed the engineered cells to both light and the chemical compounds, they were able to test which molecules helped the cells survive viral-like stress. This large-scale experiment identified about 3,500 promising compounds, which were studied further.
From these, the researchers narrowed the list down to three top candidates—IBX-200, IBX-202, and IBX-204. In lab experiments, these compounds significantly reduced infection in human cells exposed to Zika virus, herpes virus, and respiratory syncytial virus (RSV).
The compounds didn’t harm healthy cells but instead “primed” them, making their antiviral defenses stronger once an actual infection occurred.
The team then tested IBX-200 in mice infected with herpes virus. The compound reduced the amount of virus in the animals and eased symptoms, showing potential for use as a real treatment.
James Collins, senior author of the study and professor at MIT, said the goal is to create broad-spectrum antivirals. “We’re excited about this work because it shows that we can harness the stress response of host cells to fight off infection,” he explained.
Unlike traditional antivirals, which often stop working when a virus mutates, targeting the body’s own defense system could offer a more durable strategy.
Lead author Felix Wong added that the compounds don’t activate the stress pathway on their own but instead boost it when a virus has already started triggering it. “Even in the presence of a small amount of virus, if the pathway is triggered, then the antiviral response is maximized,” Wong said.
The researchers now plan to test the compounds against more viruses and explore whether similar approaches could be used to clear bacterial infections as well. The ultimate hope is that one day these compounds, or drugs based on them, could be used to treat a wide variety of viral diseases—even new ones that emerge unexpectedly.
If successful, this approach could change how we fight viruses, giving doctors a powerful new tool to stop outbreaks before they spread.
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