The study shows the unique properties of the SARS-CoV-2 virus and can explain why patients have “long-term COVID” and experience the effects of the disease for months with a feeling of fatigue and shortness of breath.
To dig deeper, researchers, led by King’s College London, analyzed the organs of 41 patients who died of Covid-19 at the University Medical Center of Trieste, Italy.
The team took samples of the lungs, heart, liver and kidneys to study the behavior of the virus.
The results showed extensive lung damage in most cases, with a profound disruption of normal lung structure and the conversion of respiratory tissue into fibrotic material in patients.
Almost 90 percent of patients showed two additional features that were unique to Covid-19 when compared to other forms of pneumonia.
Initially, the patients showed extensive blood clotting of the pulmonary arteries and veins (thrombosis).
Second, several lung cells were unusually large and had many nuclei, which resulted from the fusion of different cells into single large cells.
This formation of fused cells (syncytia) is due to the viral spike protein that the virus uses to enter the cell.
“When the protein is present on the surface of cells infected with the Covid-19 virus, it stimulates their fusion with other normal lung cells, which can be a cause of inflammation and thrombosis,” the authors wrote in one in The Lancet’s published eBioMedicine article from King’s College London in collaboration with the University of Trieste and the International Center for Genetic Engineering and Biology in Italy.
In addition, research has shown the long-term persistence of the virus genome in respiratory cells and in cells lining the blood vessels, along with the infected cell syncytia.
The presence of these infected cells can cause the major structural changes in the lungs, which can last for weeks or months and which could eventually explain “long covid”.
The study found no obvious signs of viral infection or persistent inflammation in any other organs.
“The results show that Covid-19 is not simply a disease caused by the death of virus-infected cells, but is likely the result of these abnormal cells that persist in the lungs for long periods of time,” said Professor Mauro Giacca of the British Heart Foundation Center at King’s College London.
The team is now actively testing the effects of these abnormal cells on blood clotting and inflammation, and is looking for new drugs that can block the viral spike protein that causes cells to fuse.
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