Disabling a single protein could “cure” the common cold

Disabling a single apparently non-essential protein in the cells would prevent a broad range of enteroviruses, including rhinoviruses, from developing.

Scientists at US Stanford and California Universities in Los Angeles who have achieved this breakthrough claim that these viruses cause half of colds, polio and other common diseases that can cause paralysis.

Researcher Jan Carette and his colleagues worked on human lung cells in the laboratory, as well as on mouse cells.

Landmarks

  • Infections due to colds are very common.
  • An adult suffers from two to five colds a year.
  • The common cold is an infection of the upper respiratory tract (nose, nasal passages and throat).
  • There are more than 200 viruses that can cause colds.
  • In adults, rhinoviruses, of which there are more than one hundred varieties, form the main family of viruses causing colds.

Face the problem from another angle

The viruses that cause the common cold are a headache for medicine because they quickly learn to hide from the immune system and quickly become drug-resistant.

In this study, researchers created a therapy that does not directly attack viruses, but rather targets a protein in our cells that viruses need to multiply.

You should know that a virus does not have all the equipment it needs to replicate itself. It actually depends on the cells it infects and some of their parts.

The researchers have therefore targeted a mammalian cell protein that viruses must reproduce to develop.

Their research is not yet mature enough to test humans, but it has led to complete protection in laboratory experiments.

It has also stopped viruses associated with asthma and encephalitis.

Cold or flu?

The flu and colds are respiratory tract infections and are often confused because of the similarity of their symptoms. However, the cold is more common and more commonplace than the flu, which can be very serious. Some symptoms such as fever, headache, aches, pains and nausea are mostly related to the flu.

A new approach

Scientists have used genetic editing to turn off instructions encoding a protein (called SETD3 methyltransferase) in cells.

They then exposed these modified cells to a range of enteroviruses.

The result is promising. All viruses were unable to replicate inside modified cells.

Tests were then conducted on genetically modified mice not to produce this protein. Again, viruses have not been able to replicate.

The protein in question usually plays a role in a complex scaffold within the cells of the body, called the cytoskeleton. Genetically modified mice have lived without health problems despite the absence of this protein.

As there is no question of creating genetically modified humans, the authors of this work published in the journal Nature Microbiology hope to develop a drug that can temporarily remove the protein and thus provide protection against viruses.

We must now create a molecule that would have this effect. Further work must also be done to establish the exact role of the protein in viral replication.

Well known and feared

In addition to the viruses associated with the common cold, one of the best-known and most feared enteroviruses is poliovirus. The latter causes poliomyelitis, a disease whose incidence has dropped in Canada and around the world after the creation of vaccination programs in the 1950s.

Until the advent of the vaccine, this virus was synonymous with paralysis and death.

Since 2014, another type of enterovirus, the EV-D68, has appeared in the United States and Europe. It causes acute flaccid myelitis that results in the appearance of muscle weakness in one or more limbs.

Other enteroviruses can cause encephalitis (inflammation of the brain) and myocarditis (inflammation of the heart).

Like all viruses, these enteroviruses travel easily and to replicate, they take advantage of the proteins of the cells they infect.

This work could not only be useful against colds, but also against these much more dangerous enteroviruses.

 

Related Posts

Leave a Reply

Your email address will not be published. Required fields are marked *