Winter is a season of illnesses related to colds, sore throat, runny nose and sinusitis. Scientists are now one step closer to stopping the common cold.
Newly published research has found that disabling a specific protein in our cells blocks the progression of the cold-causing virus. The new method is currently only being tested in mice, but the results show promise.
Colds are the most common infectious disease in the world. Their popularity is due to more than 200 viruses that cause colds and they can mutate, becoming resistant to drugs and vaccines. This means that even if you have caught a cold 20 times in your life and therefore, you are immune to those 20 viruses, there are still many others waiting to surprise your immune system. .
There are currently about 160 common cold viruses belonging to a group of viruses called rhinoviruses.Rhinoviruses is part of a broader group called enteroviruses , the most famous of which is polio.
In the near future, colds will no longer be a nightmare for many people in the winter.
Researchers from Stanford University and the University of California-San Francisco disabled a certain protein in mammalian cells and discovered that this prevented replication of enteroviruses.
To find out which genes could bind to the replication virus, the researchers cultured human cells in the lab and then used gene editing to disable a random gene in each cell. . They then exposed the cells to RV-C15 rhinovirus and an enterovirus called EV-C68 , which was associated with a rare disease of the spinal cord called acute soft myelitis.
The team found that cells without the enzyme coding gene (a protein that speeds up the biochemical reaction) called SETD3 prevented both viruses from multiplying to infect new cells. They then infected the disabled SETD3 cells with three rhinoviruses, one type of polio and some other enteroviruses and found that none could replicate in the cells. However, once the SETD3 gene is restored normally, the virus can replicate successfully.
Overall, viral replication was 1,000 times lower in SETD3-deficient human cells and 100-fold lower in bronchial epithelial cells, found in enzyme-deficient respiratory systems.
But how can the absence of this enzyme affect the body? Researchers bred transgenic mice that could not produce SETD3 and found that they had matured in good health and were fertile. In addition, they are immune to two types of enteroviruses that often have serious consequences, even if these viruses are injected directly into the brain.
Still far from direct human trials, this potential drug is far from being created and made available to the general public. The new discovery, however, offers hope that someday it can, allowing future generations to enjoy the winter unaffected by the common cold.