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Common refrigerants can be close, says researchers from Stanford




Teacher Jan Carette sits in the lab where he and other researchers discovered a promising way to prevent common cold viruses from multiplying. (Paul Sakuma / Stanford University)

Sneezing. Sniffling. Cough.

There's not much you can do to stop the cold besides waiting. But a new study published in Nature Microbiology may have lit the way to discover a drug that can stop the virus in its tracks, researchers say.

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

That's exactly 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 that a drug that can keep the virus away from that protein may be able to stave off your winter cold.

"There is still a long way to go," Jan Carette, associate professor of microbiology and immunology at Stanford University School of Medicine, told The Washington Post. "But I think it's an important step."

A cure for cold has been difficult for researchers, in part because about 160 strains of rhino virus can cause your sniffing, foggy head cold. To prevent influenza, researchers target only three to four influenza strains each year. Researchers have been able to create vaccines that are quite effective at targeting the flu, but it is much more difficult to detect 160 varieties of rhino virus. Add to the puzzle the speed at which viruses mutate, and it's easy to see why treating colds has long been a frustrating scientific move.

"The real problem with trying to generate a vaccine is that it hasn't worked so far," Carette said, "so it probably won't work."

Scientists know some things about how the spread of these rhinos, which belongs a genus called enterovirus The virus penetrates a host cell and uses some of its own proteins and some of the host's proteins to replicate, creating hundreds of copies of itself, which are spread to other healthy host cells and restart the process until the immune system realizes that The body is under attack and is starting to fight the infection.

"People say," The cold isn't that bad, is it? You sniff for a few days and then it's over, "Carette said.

That is 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 can also be defeated by a broad spectrum of antiviral drugs, can cause serious symptoms, including paralysis.

"When we started our research, we started with these two problems in our mind," he said

California researchers were looking for a way to inhibit the virus from spreading from cell to cell, which could eventually lead to a new antiviral drug. Carette began her quest for a possible cure for the cold by knocking out genes for possible "host proteins" one by one using CRISPR, a gene editing method that can alter specific DNA sequences from a cell or organism's genome.

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

Some of the cells contracted the virus, but others flourished.

The lack of a nasty protein consistently stopped the virus in its tracks: SETD3 . [19659017] The researchers then turned off the gene for SETD3 in healthy human lung cells, often infected by rhinovirus strains. The virus failed to multiply and spread there.

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

The 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 of trying to deal with the cold," Carette said.

Other immunology researchers said the study is promising.

"I think the quality of the work is outstanding and the various parallel studies that were conducted to prove that this really interesting and important result were also extremely well done," Alex Khromykh, a virologist and senior scientist at the Australian Research Center told infectious diseases at the University of Queensland, to The Post. "As a researcher, I would like to greet these types of studies and really support them. As a doctor or physician who wants these drugs ready tomorrow it is probably unlikely. But with the right development, it is possible to happen later. "

Although the study's results may send researchers on the path to a cure for colds, much more research is needed.

"There is a long way to go before we know if we can develop an antiviral targeting this protein. We are talking for years of work," said microbiologist Vincent Racaniello of Columbia University to Scientific American. "Just because you can take it out in mice does not mean you can take it out in humans. "

Human trials can show that SETD3 plays a more important role in our bodies than in mice and that inhibition of protein can put patients at risk, which can forcing scientists back to square one.

But Carette said he is keen to start looking for a drug that can safely inhibit the interaction between the virus and the protein SETD3.

"The reality is, even when you have the drug it takes time to go through this pipeline of preclinical and safety testing, "he said." It's usually five years if you're very optimistic, or 10 years if you're more realistic. "


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