Cold stopped by experimental approach

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Scientists believe they have found a way to fight colds and closely related viruses that can cause paralysis.

Instead of trying to attack them directly, researchers have targeted an essential protein inside our cells that viruses must replicate.

The approach gave a "complete protection" during experiments on mouse and human lung cells.

However, researchers based in the United States are not ready for testing on people.

The common challenge

Attacking colds is a major problem in medicine.

Most colds are caused by rhinoviruses, but there are about 160 different types and they mutate so easily that they quickly become drug-resistant or learn to hide from the immune system.

This has led to the idea of ​​"host-directed therapy" – essentially making our body inhospitable to cold viruses.

An individual virus does not have all the hardware needed for replication. Instead, it is necessary to infect another cell and steal some of the coins inside.

This is why scientists continue to wonder if viruses are really alive.

A team from Stanford University and the University of California at San Francisco has discovered one of the essential components for viruses.

Viral dependence

Scientists began with human cells and then used gene editing to disable the instructions contained in our DNA one by one.

These modified cells were then exposed to a range of enteroviruses, including rhinoviruses that cause colds and more dangerous viruses closely linked to polio and can cause paralysis.

All viruses were unable to replicate inside cells for which the instructions for a protein (called SETD3 methyltransferase) were turned off.

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

"The absence of this gene has completely protected mice from viral infection," said Professor Jan Carette, associate professor at Stanford.

"These mice would 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 protein on which these viruses depend normally has a role to play in the complex "scaffolding" that organizes the inside of the body's cells, called the cytoskeleton.

The results, published in the journal Nature Microbiology, showed that genetically modified mice were in good health, despite the lack of proteins for their entire lives.

When do we have treatment?

The goal is not to produce genetically modified humans, but to find a drug capable of temporarily suppressing the protein and ensuring its protection.

"We have identified a fantastic target that all enteroviruses and rhinoviruses need and depend on – eliminate it and the virus has no chance," said Professor Carette.

He added, "This is a very good first step, and the second step is to have a chemical that mimics this genetic deletion.

"I think development can go pretty fast."

The exact role of the protein in viral replication is still uncertain and will require further research.

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

Professor Jonathan Ball, a virologist from the University of Nottingham, who did not participate, said the study was "neat", but scientists should be sure the approach was safe.

"There is a growing interest in developing treatments targeting these host proteins because they can potentially overcome the mutation of the virus – one of the major barriers to developing effective broad-based antivirals.

"But, of course, the viruses are very adaptable and it is conceivable that even targeting a host does not keep them far away from their distance."

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