[ad_1]
As the summer fades, we can expect cool mornings, enjoyable evenings and, of course, vacations. But we all dread an aspect of winter: sore throat, nose drops and sore sinus headaches. But do not worry, scientists are about to end the cold, making the winter months much more bearable.
The new research, published in Nature Microbiology, revealed that disabling a specific protein in our cells halted the progression of cold viruses. It is still in its infancy – the new method has only been tested on mice and human cells in a dish – but the results are promising.
"Our grandmothers have always asked us," If you are so smart, why do not you offer a cold treatment? ", Said Dr. Jan Carette, lead author." Now we have a new way of doing this. "
The cold is the most prevalent infectious disease in the world and every winter we can expect to have up to four. Their omnipresence is that there are more than 200 cold viruses that can mutate, become drug-resistant and avoid vaccines. This means that even if you have had 20 colds in your life and are immune to these 20 viruses, there is still a lot to wait to catch your immune system by surprise.
About 160 cold viruses belong to a group of viruses known as rhinoviruses ("rhino" means "nose" in Greek). In turn, rhinoviruses are part of a larger group called enteroviruses, the most famous of which is poliovirus. Researchers at Stanford University and the University of California at San Francisco have deactivated some protein in mammalian cells and found that it prevents enteroviruses from replicating.
To determine which genes might be linked to the ability of the virus to replicate, researchers cultured human cells in the laboratory and then used gene editing to turn off a random gene in each cell. They then confronted the RV-C15 rhinovirus cells and an enterovirus called EV-C68, which is linked to a rare disease of the spinal cord called acute flaccid myelitis. Some cells managed to survive and divide.
The team found that cells lacking a gene encoding an enzyme (a protein that accelerates biochemical reactions) called SETD3 were able to prevent both viruses from replicating to infect new cells. They then infected cells with a deactivated SETD3 gene with three rhinoviruses, a poliovirus and a handful of other enteroviruses and found that none of them could replicate in cells. However, when the SETD3 gene has been restored to normal, the viruses could replicate successfully.
Globally, viral replication was 1000-fold lower in human cells lacking SETD3 and 100-fold lower in bronchial epithelial cells, present in the respiratory system, lacking the enzyme.
But how could an absence of this enzyme affect the body? The researchers raised genetically modified mice that could not produce SETD3 and found that they had reached adulthood in good health and were fertile. In addition, they were immune to two enteroviruses that normally have fatal consequences, even if these viruses were injected directly into their brains.
The team also realized that the viruses did not use the part of the SETD3 protein used by human cells. "This gives us hope that we will be able to develop a drug with broad antiviral activity not only against the common cold, but perhaps against all enteroviruses, without even disrupting the normal functioning of SETD3 in our cells," said Carette.
Still far from the tests on humans, this potential drug is still far from being created and made available to the masses. However, the new discovery gives hope that it will one day, allowing future generations to enjoy a cold winter cold.
[ad_2]
Source link