As summer slowly fades away, we can look forward to crisp mornings, cozy evenings, and, of course, the holidays. But there’s one aspect of winter we all dread: sore throats, dripping noses, and painful sinus headaches. But fear not, scientists are one step closer to stopping the common cold in its tracks, making the winter months a whole lot more bearable.
The new research, published in Nature Microbiology, found that disabling a specific protein in our cells halts the progression of cold viruses. It’s still very early days – the new method has only been tested out on mice and human cells in a dish – but the findings show promise.
“Our grandmas have always been asking us, ‘If you’re so smart, why haven’t you come up with a cure for the common cold?’” said senior author Dr Jan Carette. “Now we have a new way to do that.”
The cold is the most common infectious illness in the world, and each winter we can expect to catch up to four of these irksome viruses. Their pervasiveness is thanks to the fact that there are over 200 cold viruses and they can mutate, becoming resistant to medicines and dodging vaccines. This means that even if you’ve had 20 colds in your life, and you’re therefore immune to those 20 viruses, there are still plenty more waiting to catch your immune system by surprise.
About 160 common cold viruses belong to a group of viruses known as the rhinoviruses (“rhino” is Greek for nose). In turn, rhinoviruses are part of a wider group known as enteroviruses, the most famous of which is poliovirus. Researchers from Stanford University and the University of California-San Francisco disabled a certain protein in mammalian cells and found that this stopped enteroviruses from replicating.
To work out which genes might be linked to the viruses’ ability to replicate, the researchers grew human cells in the lab and then used gene editing to disable a random gene in each cell. They then confronted the cells with the rhinovirus RV-C15 and an enterovirus called EV-C68, which is linked to a rare disease of the spinal cord called acute flaccid myelitis. A few cells managed to survive and divide.
The team found that cells devoid of a gene that codes for an enzyme (a protein that speeds up biochemical reactions) called SETD3 managed to prevent both viruses from replicating to infect new cells. They then infected cells with a disabled SETD3 gene with three rhinoviruses, a poliovirus, and a handful of other enteroviruses and found that none could replicate within the cells. However, when the SETD3 gene was restored to normal, the viruses could replicate successfully.
Overall, viral replication was 1,000 times lower in human cells lacking SETD3, and 100 times lower in bronchial epithelial cells, which are found in the respiratory system, lacking the enzyme.
But how might an absence of this enzyme affect the body? The researchers bred genetically modified mice that could not produce SETD3 and found that they made it to adulthood in good health and were fertile. In addition, they were immune to two enteroviruses that normally have fatal consequences, even if these viruses were injected directly into their brains.
The team also realized that the viruses don’t use the part of the SETD3 protein used by human cells. “This gives us hope that we can develop a drug with broad antiviral activity against not only the common cold but maybe all enteroviruses, without even disturbing SETD3’s regular function in our cells,” said Carette.
Still far from human trials, this potential drug is a long way from being created and made available to the masses. However, the new discovery provides hope that it one day might be, allowing future generations to enjoy winter unplagued by the common cold.
