cold

How to treat colds? Target the person, not the virus

pharmafile | May 15, 2018 | News story | Research and Development biotech, common cold, drugs, pharma, pharmaceutical 

Researchers from Imperial College London have discovered how to interfere with one of the building blocks that allows the common cold to replicate rapidly in the human body.

In a different way of approaching the complicated issue of trying to combat the rhinovirus, the therapy works by targeting the host’s cells instead of the virus.

In particular, it targets the N-myristoyltransferase (NMT) protein, which the virus needs to construct a protein ‘shell’ to protect the virus genome.

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The compound was discovered during researchers’ investigations into new ways of targeting malaria; drug screening showed two compounds had the potential to block the NMT protein and though alone they were ineffective, when combined they were able to produce the desired results.

As all strains of the cold virus use the same human protein to duplicate, treatment with the compound, IMP-1088, could potentially protect humans from all forms of the rapidly changing cold virus and even work on similar viruses, such as polio and foot and mouth disease.

The cold virus is so difficult to pin down with a treatment because there are such a number of varieties and they are able to evolve very quickly.

Lead researcher Professor Ed Tate, from the Department of Chemistry at Imperial, said: “The common cold is an inconvenience for most of us, but can cause serious complications in people with conditions like asthma and COPD. A drug like this could be extremely beneficial if given early in infection, and we are working on making a version that could be inhaled, so that it gets to the lungs quickly.”

An added benefit to this potential treatment is that the onset of action, in cell samples, was rapid – preventing the spread of the cold virus only one hour after the introduction of the treatment.

This allowed researchers to show that it could be effective whether introduced an hour before, during infection or up to two after the virus had taken hold. A major question that would have to be answered would be how to extend the duration of time the treatment could be effective for, given that cold symptoms generally do not emerge until one or two days after infection.

The next stage is to take the research into animal studies to determine whether the treatment has any side-effects that could make using it in humans dangerous.

Ben Hargreaves

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