Home » The scientist, ‘discovered mechanism could also be involved in long Covid’ has already started experimentation in India

The scientist, ‘discovered mechanism could also be involved in long Covid’ has already started experimentation in India

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Milan, April 7 (beraking latest news Health) – It is a drug used for more than 50 years for intestinal infections, and according to scientists working between London and Trieste, it can block the harmful effects that the Spike protein of Sars-CoV-2 causes to cells and damage caused by Covid-19 to the lungs. The study is by a group of researchers from King’s College London, the University of Trieste and the Trieste Center for Genetic Engineering and Biotechnology (Icgeb). Published today in the journal ‘Nature’, the work has identified the mechanism that leads to the fusion of cells infected with Sars-Cov-2 and a drug capable of blocking this process, now the protagonist of an experiment in India.

Through a laboratory screening of over 3 thousand drugs already approved for the treatment of various diseases, the group of Italian and English researchers led by Mauro Jacket, professor at the University of Trieste, professor of Cardiovascular Sciences at King’s College London and head of the Laboratory of molecular medicine of the ICGEB, found that the pesticide niclosamide, is able to block the harmful effects that the Spike protein of Sars-CoV-2 causes to cells.

The same group of researchers in November last year in an article published in ‘Lancet eBioMedicine’ had discovered that the lungs of patients who died from Covid-19, in addition to showing extensive damage and the presence of clots that block the circulation of the blood, contain a large number of abnormal cells, very large and with many nuclei, infected with the virus even after 30-40 days of hospitalization. These abnormal cells are generated by the ability of the coronavirus Spike protein to stimulate fusion between infected cells and neighboring cells.

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“We are very satisfied with our results – says Jacket – for at least two reasons. First, because we have discovered a completely new mechanism, activated by the Spike protein and important for the virus. Our research shows how Spike activates a family of proteins in the cell. called TMEM16, which are essential for cell fusion. Second, because this mechanism also underlies platelet activation, and could therefore also explain why 70% of patients with severe Covid-19 develop thrombosis. And now we know that there is at least one drug, niclosamide, capable of blocking this mechanism “.

The drug, synthesized in the 1970s, has been used since 1982 for the treatment of intestinal infections due to tapeworms. The new study shows how, by inhibiting TMEM16 and cell fusion, it can also block virus replication. Based on these results, a clinical trial on 120 patients has already started in India, where the infection is still widespread and niclosamide is being administered to a group of patients hospitalized with Covid-19, the experts explain. This is a trial that has just started, they point out, and therefore it will be of fundamental importance to wait for the results over the next few months to confirm the effectiveness of the drug.

“I think this research is important – continues Jacket – also because it shifts attention from the attempt to block the multiplication of the virus, as has been tried so far with some drugs, with little success, to that of inhibiting the damage caused to the virus. organism from infected cells. I am increasingly convinced that Covid-19 is a disease caused not by the simple destruction of cells infected by the virus, but by the persistence of these cells in the body for long periods of time. The mechanism we have discovered could therefore also be involved in the development of the so-called long Covid, or explain the difficulty that many patients have in recovering after the disease “.

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The research was conducted in the laboratories directed by Jacket at the School of Cardiovascular Medicine & Sciences of King’s College London, with Icgeb and the University of Trieste, and with the collaboration of the Institute of Pathological Anatomy of the University of Trieste and the support of the professors of the Friuli University Rossana Bussani (pathological anatomy) and Chiara Collesi (molecular biology), but also with the collaboration of other research groups of King’s College London, Imperial College London and the Institute of Biophysics of the Cnr of Trento.

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