Stuffy Noses Begone — Researchers Are One Step Closer To Eliminating The Common Cold
As someone who reaches for a turmeric-ginger shot at the very mention of cold season, you could say I have a pretty big (and completely valid!) fear of feeling sick. With the common cold being one of the world's most prevalent infectious illnesses (colds cost $40 billion a year for the United States), I know I'm not alone in my aversion to coughs and congestion.
What's exciting is that there might be a silver lining for those of us with a fear of cold season—in a recent study published in Nature Microbiology, scientists found that they could disable a noncritical protein in cells that all enteroviruses and rhinoviruses appear to need in order to replicate.
First, what do these viruses mean?
Around half of common colds can be categorized as rhinovirus infections, which are highly mutation-prone and quick to develop drug resistance, which could explain why you could get another cold just after battling your last week of bed rest. Enteroviruses, on the other hand, tend to be a little more serious—these include infections such as asthma, encephalitis, and polio.
In this study, deficiency is a good thing.
During the study, the scientists first used gene editing to randomly disable a single gene in human culture cells. After a long (and probably grueling) process, they found that when the gene with the code SETD3 was eliminated, several types of enteroviruses were unable to replicate. Once the SETD3 was restored, those enteroviruses were more than capable of infecting the same cells. Clearly, a deficiency in this specific gene is significant for viral success.
While this human culture study proved significant, the scientists took their findings a step further and studied a sample of bioengineered mice. These mice grew up deficient in the gene, SETD3, yet they remained healthy and fertile into adulthood. The only difference was that when they were injected with two specific enteroviruses (which can cause paralysis and fatal inflammation of the brain), they remained unaffected.
What could this mean for us and our cold season?
"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?'" senior author of the study Jan Carette, Ph.D., revealed in a news release.
While much more research is needed in order for this science to be deemed a cure, it's especially interesting that a protein that's so significant for blocking viruses is seemingly noncritical for our daily lives. Now that they've identified the gene that could stop these viruses from replicating, the next step for scientists would be to develop a drug that disables this specific protein in our cells.
"Traditional antiviral drugs target the virus itself," Carette said. "But the virus is very smart, and it can mutate its way around it. What we do is make the host inhospitable for these viruses. So it's much more difficult for these viruses to mutate around." Although it might be a while before we see these virus-blocking drugs hit the shelves of our local CVS stores, it's exciting that scientists have found a way to work around these particularly smart viruses and their drug-resistant capabilities.
Unfortunately for us, this year's cold season is quickly approaching—much faster than this research will most likely commercialize. For now, it's probably best to keep that immunity tea and turmeric juice on hand. Until we can safely say that cold season is a thing of the past, sticking to your traditional vitamin C-heavy regimen is your best bet.
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