They discovered the “Achilles heel” of the coronavirus to prevent it from multiplying in the body

While many countries are trying unsuccessfully to vaccinate most of their populations to overcome the second waves of the pandemic in different territories, a recent scientific discovery could be the starting point for the study of effective drugs at the time of treatment of COVID-19 disease caused by the novel coronavirus.

Researchers at the Federal Polytechnic University of Zurich, Switzerland, they discovered an important “weak point” of the coronavirus which causes COVID-19 with which its multiplication can be inhibited and thus pave the way for the development of antiviral drugs that take advantage of this weakness.

As reported by Swiss television RTS, the scientific team, with the collaboration of experts from the universities of Bern, Lausanne and Cork, in Ireland, has reached find a theoretical method to slow down the protein production mechanism that could be the basis of future drugs against the SARS-CoV-2 coronavirus

The brake on protein production would reduce viral replication of SARS-CoV-2 in infected cells, a hitherto unknown “Achilles heel” in a coronavirus against which very few drugs were effective, science has emerged. therefore concentrated on the development of vaccines and not so much in therapies.

As Swiss and Irish scientists have explained, Their discovery is based on the fact that cells produce proteins thanks to one of its elements, the ribosome, which synthesizes them by reading RNA in sequences of three letters.

In order to replicate in an infected cell, viruses need the ribosome to have an abnormality in reading the genetic code of RNA, called a “frame shift”, whereby it reads only one or two letters of acid. ribonucleic in a sequence.

The coronavirus that causes COVID-19 and the HIV that causes AIDS need these ‘frame changes’, usually rare in human cells, to reproduce, so any component that manages to ensure that this incorrect reading of the RNA never produced can significantly weaken the virus.

“Generally, treatments for viral infections can target the virus, host, or underlying symptoms of the infection.. Antiviral treatments work by interrupting the viral life cycle. For SARS-CoV-2, the life cycle can be divided into three stages: entry and trafficking of the host cell, replication of the viral genome, and packaging and exit of new virions ”, emphasize the researchers in the journal Science.

According to the scientists, an alternative antiviral approach is to “target host cell pathways essential for virus replication, such as protein synthesis.” Viruses are completely dependent on the host for translation and have developed a variety of ways to exploit these machines for their use. In human cells, translation can be divided into four phases: ribosome initiation, elongation, termination and recycling.

The study found this route to attack the virus, although it did not specify which particular component or drug could eliminate incorrect RNA readings, which would now be left in the hands of pharmaceutical researchers.

In addition, many viruses depend on similar host spreading pathways, which gives some antivirals a broad spectrum of activity against multiple viruses. In fact, in practice, many studies of COVID-19 drugs constituted what is considered a ‘retest’, that is, evaluating the use of already approved drugs for other purposes – or combinations of these – to treat the novel coronavirus, suggesting that antivirals discovered in the race to treat COVID-19 could be useful for future outbreaks.

Despite the launch of vaccines in several countries, the discovery of antivirals to treat SARS-CoV-2 remains important. The emergence of SARS-CoV-2 variants that may be less sensitive to current vaccines is already raising concerns.

(With information from Efe)

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