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The common cold is stopped by an experimental approach



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Scientists believe they have found a way to stop the common cold and closely related viruses that can cause paralysis.

Instead of trying to attack them directly, the researchers focused on a major protein in our cells that viruses need to replicate.

The approach gave "full protection" in experiments on human mice and lung cells.

However, American researchers are not ready for human testing.

The challenge of the common cold

Dealing with the common cold is a serious problem in medicine.

Most colds are caused by rhinoviruses, but there are about 1

60 different species and they mutate so easily that they quickly become drug resistant or learn to hide from the immune system.

This led to the idea of ​​"host-targeted therapy" – essentially rendering our bodies inhospitable to cold viruses.

The individual virus does not have everything needed for replication. Instead, it depends on infecting another cell and stealing some of the parts inside.

That's why scientists are still arguing whether viruses are really alive.

A team at Stanford University and the University of California San Francisco discovered one of the components on which viruses depend.

Viral Dependency [19659009] Scientists started with human cells and then used gene editing to rule out instructions inside our DNA one by one.

These modified cells were then exposed to a number of enteroviruses – this includes rhinoviruses that cause the common cold and more dangerous viruses that are closely related to polio and can cause paralysis.

All viruses could not replicate inside the cells in which protein instructions (called methyltransferase SETD3) were excluded.

The scientists then created genetically modified mice that were unable to produce this protein.

"The absence of this gene protected the mice completely from a viral infection," Associate Professor Jan Caret of Stanfor told the BBC.

"These mice will always die [without the mutation] but they survived and we saw a very strong reduction in viral replication and very strong protection."

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the common cold turned out to be incredibly difficult to stop

The protein on which these viruses depend usually plays a role in the complex "scaffold" that organizes the interior of the cells of the body called the cytoskeleton.

The results published in the journal Nature Microbiology show that genetically modified mice were healthy, although they lacked protein throughout their lives.

When Do We Receive Treatment?

The plan is not to produce genetically modified humans, but to find a drug that temporarily suppresses the protein and provide protection.

"We have set a fantastic goal that all enteroviruses and rhinoviruses require and depend on. Take it away and the virus really doesn't stand a chance, "says Prof. Karet.

He added: "This is a really good first step – the second step is to have a chemical that mimics this genetic deletion.

"I think development can proceed relatively quickly."

Exactly what role the protein plays in viral replication is still uncertain, and further study will be needed.

For most people, the common cold is more a nuisance than a threat to their health, but in asthmatics it can aggravate their symptoms a lot and some of the enteroviruses can cause paralysis if spread to the brain.

Prof. Jonathan Ball, a virologist at the University of Nottingham who did not participate in the study, said the study was "clean" but scientists should be sure the approach was safe.

"There is increasing interest in developing treatments that target these host proteins, as they can potentially overcome the mutation of the virus, one of the major barriers to the development of effective widely active antiviral agents.

"But, of course, the viruses are very adaptable, and even host-targeted treatments may not keep them at bay for long."

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