Common Cold

Common Cold Stopped By Experimental Approach

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

Instead of trying to attack them directly, the researchers targeted an essential protein inside our cells which the viruses need to replicate.

The approach gave “complete protection” in experiments on mice and human lung cells.

However, the US-based researchers are not ready for trials in people.

The common-cold challenge

Tackling the common cold has been a massive problem in medicine.

Most colds are caused by rhinoviruses, but there are around 160 different types and they mutate so easily they rapidly become resistant to drugs, or learn to hide from the immune system.

A team at Stanford University and the University of California, San Francisco, found one of the components which the viruses were dependent upon.

Viral dependency

Scientists started with human cells and then used gene-editing to turn off instructions inside our DNA one-by-one.

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

The findings, published in the journal Nature Microbiology, showed the genetically modified mice were healthy, despite lacking the protein for their whole lives.

When do we get a cure?

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

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 go relatively quickly.”

Exactly what role the protein plays in the viral replication is still uncertain, and will require further research.

“There is increasing interest in developing treatments that target these host proteins, because it can potentially overcome virus mutation – one of the major barriers to developing effective broadly active antivirals.

“But of course, viruses are very adaptable and it is conceivable that even a host-targeting treatment might not keep them at bay for long.”