How Spike stimulates cell fusion
These abnormal cells are generated by the ability of the coronavirus Spike protein to stimulate fusion between infected cells and neighboring cells. Stimulated by these observations, the researchers have now discovered the mechanism that allows cells to fuse and found a drug that can block this process.5The latest of24+
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«We are very satisfied with our results – says Mauro Jacket – for at least two reasons. First, because we have discovered an entirely new mechanism, activated by the Spike protein and important to the virus. Our research shows that Spike activates a family of cell proteins, 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 “.
Experimentation in India is underway
Niclosamide is a drug synthesized in the 1970s and used since 1982 for the treatment of intestinal infections due to tapeworms. The new study shows how this drug, by inhibiting Tmem16 and cell fusion, also blocks the replication of the virus.
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. This is a trial that has just started, 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 they have so far tried to do with some drugs, with little success, to that of inhibiting the damage caused to the 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, that is, explain the difficulty that many patients have in recovering after the disease “.
The research was conducted in the laboratories directed by Professor Jacket at the School of Cardiovascular Medicine & Sciences of King’s College London, the International Center for Genetic Engineering and Biotechnology of Trieste and the University of Trieste, with the collaboration of the Institute of Pathological Anatomy of the University of
Trieste thanks to the support of the professors of the University of Trieste Rossana Bussani, professor of pathological anatomy and Chiara Collesi, professor of molecular biology, and with the collaboration of other research groups of King’s College London, Imperial College London and of ‘Institute of Biophysics of the Cnr of Trento.