The formation of syncytia, which Jacket compares to “large lakes of cells” is the work of the spikes. This also happens with the crown tip of another coronavirus: that of MERS, but not in the first Sars of 2002-2003. With Sars-Cov-2 researchers (in particular Rossana Bussani, an expert in pathological anatomy at the University of Trieste) had noticed the phenomenon by performing autopsies on the first wave of Covid victims, fully harnessed to avoid contagion.
“Never seen anything like it,” said Jacket at the time. “Syncytia obstruct the circulation of blood in the lungs and cause the secretion of water, which causes edema and prevents breathing.” In severe cases, the clusters of cells do not disappear even weeks after the infection. “We have seen them in the lungs of people who died after four months of Covid. Even in those who had a negative swab and were apparently cured”. If so far the storm of the immune system was the main suspect, for the extensive damage to the respiratory system, now Jacket’s group introduces the presence of a new weapon, through which the coronavirus turns into a killer.
Today, after describing the problem, researchers from London and Trieste also suggest the solution: a laboratory robot took 3,000 test tubes with 3,000 drugs already in use for various diseases and observed their behavior in the face of syncytia. One in particular proved adept at blocking them, as the team explains in an article in Nature. It is called niclosamide, has been used for more than 50 years against some intestinal parasites such as tapeworms and is cheap. “It blocks those mechanisms that occur on the membrane of the cells by the spike and lead them to fuse. We have started the first tests in India. We are ready to extend them also in Europe” explains Jacket. “But in Britain there aren’t many serious patients in hospital for extensive trials now.” Niclosamide blocks the action of the crown tip, which promotes cell fusion, but also has a direct action against the virus. “We observed it in vitro,” says the scientist.
The same mechanism by which the spike pushes cells to form agglomerates can be used to explain why thrombus formation is so serious and widespread in Covid: “The spike, this very particular protein of the coronavirus, triggers a mechanism that is able to amplify their activation up to 10 thousand times. By activating the chlorine channels on the cell membrane it causes the secretion of water, thus explaining symptoms such as diarrhea and pulmonary edema. It then inactivates the smell and taste neurons. Some of the more mysterious effects of the coronavirus can perhaps be understood, revealing in detail what is the action of the tip of the crown on our cells. ”