Could we be one step closer to a cure for the common cold?
Viruses typically "hijack" NMT from human cells to construct the capsid - or protein shell - to protect the virus genome.
By inventing a novel way to combine the two, they created a molecule, codenamed IMP-1088, which is more than a hundred times more potent than previous molecules targeting the protein in humans.
Because this kind of strategy targets the human protein that helps the virus replicate it means that any treatment developed should be effective against different strains of the virus that emerge, making this a truly universal common cold cure. And as the molecule affects the protein rather than the virus, it is unlikely the agents will become resistant to it.
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Tate highlighted that while the common cold is an inconvenience for most people, it can cause serious complications for people with conditions such as asthma and chronic obstructive pulmonary disease, which includes emphysema and chronic bronchitis.
Previous attempts to create drugs which engage with human cells rather than the virus itself have failed because they were found to be too risky.
Early lab-based tests with human cells have shown the molecule's ability to completely block multiple strains of cold virus, and the team hope to move to animal and then human trials.
Ed Tate, professor of chemical biology at Imperial College London and co-author of the study, said in a statement: "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". However, initial lab results suggest the new molecule does not negatively affect human cells. In these human cell tests there was no sign of broader cytotoxicity and this NMT strategy could have applications for viral infections other than the common cold, including foot and mouth disease and poliovirus.
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Writing in the journal Nature Chemistry, a team of researchers based around the United Kingdom report how they looked at molecules that interact with a human enzyme that attaches a type of fatty acid molecule on to proteins. But attempts to thwart the pathogen by vaccination or antiviral drugs face a number of difficulties - not least because the virus comes in many forms and can mutate rapidly leading to drug resistance.
But the new approach could be more successful because it does not target the virus directly.
"While this study was conducted entirely in vitro, i.e. using cells to model rhinovirus infection in the laboratory, it shows great promise in terms of eventually developing a drug treatment to combat the effects of this virus in patients".
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