08.04.2021 – 08.00 – A drug developed in the seventies, niclosamide, used for intestinal infections, could potentially reduce the damage caused by the protein Spike of Sars-CoV-2 to cells.
An Anglo-Italian group of researchers from King’s College London, the University of Trieste and the Center for Genetic Engineering and Biotechnology (ICGEB) in Trieste discovered this after screening over three thousand drugs.
In India, where the spreading of the Coronavirus is still out of control, a mass research has been launched to confirm whether the use of niclosamide could actually help patients, as well as avoid long-term damage. The Spike protein of Covid-19 stimulates fusion between infected and neighboring cells generating abnormal, large multinuclear cells.
This process occurs even after the infection, 30-40 days after hospitalization.
It was researchers from Trieste who made the discovery last November, after a series of studies on the lungs of deceased patients who had exhibited clots capable of blocking blood circulation and tearing the lung tissues. The potential of niclosamide to stop this fusion between healthy and diseased cells could be of great importance in the fight against Covid-19. “We are very pleased with our results,” summarized Mauro Giacca, professor at the University of Trieste and professor of Cardiovascular Sciences at King’s College London, “for at least two reasons. First, because we have discovered a wholly 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, that 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 we now know that there is at least one drug, niclosamide, that can block this mechanism.”
“I think this research is important” — continues Mauro Giacca — also because it shifts the focus from trying to block the multiplication of the virus, as we have tried to do so far with some drugs, with little success, to inhibiting the damage caused to the body by the infected cells.
I am increasingly convinced that Covid-19 is a disease caused not by the simple destruction of cells infected with the virus, but by the persistence of these cells in the body for long periods of time.
The mechanism we discovered could therefore also be involved in the development of so-called long Covid, i.e., explain the difficulty many patients have in recovering after the disease.”
[The research, published in the prestigious journal Nature, was conducted in the laboratories directed by Professor Giacca at the School of Cardiovascular Medicine & Sciences of King’s College London, the International Center for Genetic Engineering and Biotechnology in Trieste and the University of Trieste, with the Institute of Pathological Anatomy of the University of Trieste thanks to the support of Rossana Bussani, professor of pathological anatomy, and Chiara Collesi, professor of molecular biology, and with the collaboration of other research groups from King’s College London, Imperial College London and the Institute of Biophysics of the CNR in Trento]