New experimental approach could stop common cold
Scientists believe they may have found a way to stop the common cold as instead of attacking the virus directly, researchers could target an essential protein found inside our cells which the viruses require to replicate.
In experiments on mice and human lung cells the approach gave “complete protection” – however the US-based researchers are not currently yet ready for trials in people.
Tackling the common cold has been a huge problem in medicine. Most colds are caused by rhinoviruses, but there are over 160 different types and they mutate, rapidly becoming resistant to drugs or having the ability to hide themselves from the immune system.
The new ‘host-directed therapy’ essentially makes our bodies inhospitable for the cold virus.
Scientists started with human cells and then used gene-editing to turn off instructions inside our DNA one-by-one. The modified cells were then exposed to a range of enteroviruses – this includes the rhinoviruses as well as more dangerous ones that are related to polio and can cause paralysis.
All the viruses were unable to replicate inside cells which had the instructions for a protein (methyltransferase SETD3) switched off.
The researchers also then created genetically modified mice which were completely unable to produce that protein which in turn completely protected them from viral infection.
Jan Carette, from Stanford, added: “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.”
The findings were published in the journal Nature Microbiology, showing the genetically modified mice were healthy, despite lacking the protein their whole lives.
The plan now is not to produce genetically modified humans, but rather to find a drug which can temporarily suppress the protein and provide protection.
Virologist, Professor Jonathan Ball at the University of Nottingham said: “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.”