A new, experimental approach can help treat colds

Autumn is a golden time. She is also loved by pharmaceutical companies and manufacturers of fuflomycin. And all because catching a cold at this time of the year is not difficult. In our society, it is not customary to pay close attention to the common cold. As a rule, most colds continue to go to work and attend educational institutions. Thus, they spread the infection. However, no matter how innocuous a cold might seem to us, scientists have been struggling for years with the problems associated with its treatment. Fighting a cold is a huge medical problem. Recently, scientists said they discovered a new way to defeat her.

In autumn you need to be especially attentive to yourself

What is a cold?

The common cold is a general concept thatcombines a number of symptoms, including an upset respiratory tract. In most cases, a rhinovirus of the genus Rhinovirus causes a cold. They are characterized by symptoms such as excessive discharge from the nose, sore throat and a slight increase in temperature. In fact, there are at least 160 types of rhinoviruses. However, the biggest problem is that these viruses mutate very quickly and often become drug resistant. Sometimes they become so resourceful that they learn to hide from the immune system.

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So rhinovirus looks under a microscope

Due to the huge amount of constantly arisingmutations, finding a cure for the common cold is incredibly difficult. That's why experts say that most drugs sold as a cold medicine do not work. According to doctors, a cold goes away with or without medicine in about seven days. However, the main danger of a cold is complications. If you neglect your health, the most common cold can result in serious health consequences.

How to beat a cold?

All of the above prompted scientists to thinkthat it’s not necessary to treat the cold itself, but its owner. That is, with you. Scientists are thinking about how to make the human body unfavorable for viruses. Due to the fact that a single virus does not have all the necessary means for copying, its distribution depends on the infection of other cells and the theft of some internal constituent cells. Recently, a team of scientists from Stanford and California universities has found one of the components on which the reproduction of viruses depends.

Scientists began work with human cells,resorting to editing the genome. Specialists wanted to turn off the instructions that make some genes work in turn. Subsequently, the resulting modified cells were deliberately infected with a number of enteroviruses, including rhinoviruses that cause colds, and more dangerous viruses that are closely associated with polio and can cause paralysis. As a result, scientists achieved what they wanted — viruses embedded in edited cells could not multiply. According to experts, by editing, they “turned off” the production of protein in the cells, with the complex name methyltransferase SETD3.

In fact, not everyone can easily stand a cold

Then scientists brought genetically modifiedmice that were completely unable to produce this protein. In an interview with BBC News, one of the authors of the study, Jan Carett, said that the absence of this gene completely protected mice from viral infection. Results published in the journal Nature Microbiology showed that genetically modified mice remained healthy throughout their lives, despite the absence of SETD3 methyltransferase protein.

When will we get the medicine?

Scientists don't need to develop a medicinegenetically modified people. The plan is not to find a cure that can temporarily suppress protein and provide protection against viruses. According to Professor Carett from Stanford University, it’s worth removing the protein needed by the viruses and that’s all - rhinoviruses and enteroviruses will have no chance.

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It should be understood that this is a very important first step.in the fight of a person with a cold. However, there is still a lot of work ahead. Researchers note that at the moment, the role of protein in virus replication remains unclear, so further research will be required. A separate comment was made by Professor Jonathan Ball, a virologist at the University of Nottingham. He did not participate in the study. In his opinion, the study was “neat”, but scientists must be sure that their approach is safe. Also, do not forget that viruses adapt very quickly, so sooner or later they will find a way to penetrate organisms that do not produce SETD3 methyltransferase protein.