By Katie Shepherd

The Washington Post

There’s not much you can do to stop the common cold except wait it out.

But a study published in Nature Microbiology may have lit the path to discovering a drug that can stop the virus in its tracks, scientists say.

Researchers in California recently discovered a protein needed for the viruses that cause the common cold to spread inside your body. Get rid of the protein, get rid of the virus.

That’s just what scientists at Stanford University and the University of California in San Francisco did, first in human cancer cells, then in lung cells and finally in live mice. The results of their study suggest a drug that can keep the virus away from that protein may be able to stave off your winter cold.

“There’s still a long road to go,” Jan Carette, an associate professor of microbiology and immunology at Stanford University School of Medicine, told The Washington Post. “But I do think it’s an important step.”

A cure to the common cold has been elusive to scientists, in part because about 160 strains of rhinovirus can cause your sniffling, foggy head cold. To prevent the flu, by comparison, scientists target only three to four strains of influenza each year. Scientists have been able to create vaccines that are fairly effective at targeting influenza, but going after 160 varieties of rhinovirus is much more difficult. Add to the puzzle the speed at which viruses mutate, and it’s easy to see why treating the common cold has long been a frustrating scientific enigma.

“Really the trouble in trying to generate a vaccine is that has not worked so far,” Carette said, “so it probably won’t work.”

“People say: ‘The common cold is not that bad, right? You sniffle some days, and then it’s over,’” Carette said.

That’s largely true, but for a few people, it can be a serious illness. Those with severe asthma can endure dangerous complications from the virus. And some other rare enteroviruses, which might be defeated by a broad-spectrum antiviral drug, can cause severe symptoms, including paralysis.

“When we started our research, we started with those two problems in our mind,” he said.

The California scientists searched for a way to inhibit the virus from spreading from cell to cell, which could eventually lead to a new antiviral drug. Carette started his hunt for a possible cure to the common cold by knocking out genes for possible “host proteins” one by one using CRISPR, a gene-editing technique that can alter specific DNA sequences from a cell or organism’s genome.

Carette’s team knocked out a different gene in thousands of cancer cells until they had systematically deleted each gene in the human genome. Each cell lacked one gene and one corresponding protein. Then, his team exposed the cells to two enteroviruses.

Some of the cells succumbed to the viruses, but others flourished.

The absence of one obscure protein consistently stopped the virus in its tracks: SETD3.

The researchers then turned off the gene for SETD3 in healthy human lung cells, which are often infected by rhinovirus strains. The virus failed to multiply and spread there.

Finally, Carette said, they used a live mouse to test whether an organism without the protein could avoid the virus. Scientists injected the mice with an enterovirus with effects similar to polio. Unaltered mice deteriorated until they died of paralysis caused by the virus. But the SETD3-deficient mice survived.

That missing protein appears to be important for pregnant mice and may play a role in uterine contractions, but was otherwise unnecessary for healthy mice, the researchers found.

“We definitely have a new and exciting way to try to tackle the common cold,” Carette said.

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