Scientists have used gene-editing technology to suppress the production of a protein which is key to the replication of enteroviruses, including those that cause the common cold, as well as more life-threatening viruses related to polio that can cause paralysis. Experiments showed that mice, as well as human lung cells cultured in the lab, could not be infected by the common cold after the protein’s production was shut down.

The common cold is an upper respiratory viral infection caused by an adenovirus, rhinovirus or coronavirus. Unlike the flu, for which there are vaccines, the common cold is caused by more than 150 different viruses. Not only is there a lot of variability, the viruses can also mutate rapidly, thereby making vaccines useless. For this reason, you’ll often hear that there’s no cure for the common cold — not for the moment at least.

But, a new study published in the journal Nature Microbiology suggests that the prospect of curing the common cold isn’t so far-fetched.

Researchers at Stanford University and the University of California, San Francisco went for a different approach than other groups. Instead of boosting the immune system, the researchers decided that they would be better off destroying the logistics of rhinoviruses.

Viruses need to infect host cells where they hijack biological machinery in order to replicate. Otherwise, they cannot replicate like a normal biological cell would. This is one of the reasons why most scientists claim that viruses aren’t really alive.

The researchers knew that viruses that cause the common cold, as well as other viral infections, require a protein called methyltransferase SETD3 in order to replicate. Starting with human cells, the researchers edited the gene that is responsible for expressing the protein, turning it off. When the modified cells were exposed to a range of enteroviruses, the viruses could not replicate inside them.

Next, the researchers turned off the gene in mice, and they, remarkably, became protected against the viruses. This showed that shutting off the protein’s production staves off the common cold in a live animal.

The SETD3 protein’s role is to help build the ‘scaffold’ for the cytoskeleton — a structure that helps cells maintain their shape and internal organization. But, despite lacking this protein in their cells, the mice looked healthy for the rest of their lives. Meanwhile, mice which lacked the mutation that turned off the protein’s production died off the illnesses caused by the viral infections.

“We have identified a fantastic target that all enteroviruses and rhinoviruses require and depend on. Take that away and the virus really has no chance,” Jan Carette, a professor at Stanford and lead author of the new study, told the BBC.

Genetically modifying humans to block the SETD3 protein is a much too hazardous affair, let alone unethical. However, it is possible to replicate the mutation’s effect chemically using a drug or some other form of therapy. Isolating such a chemical is the team’s next immediate goal.

In the future, research will also have to establish the safety of switching off this gene before scientists perform any clinical trials on humans.