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Research on deceased COVID-19 patients has shed light on possible lung damage caused by the virus.
The study published today (November 3, 2020) in The Lancets eBioMedicine of King’s College London in collaboration with the University of Trieste and the International Center for Genetic Engineering and Biology in Italy shows the unique properties of the SARS-CoV-2 virus and can explain why patients suffer from “long-term COVID”.
Symptoms such as blood clotting and loss of smell and taste can occur in patients with COVID-19. Some who survive the infection may experience the effects of the disease – known as “long COVID” – for months with a feeling of fatigue and shortness of breath. There are a limited number of studies that have analyzed the organs of COVID-19 patients, which means that the characteristics of the disease are still largely unknown.
At the start of the pandemic, researchers analyzed the organs of 41 patients who died of COVID-19 at the University Hospital of Trieste (Italy) from February to April 2020. The team took samples of lungs, heart, liver and kidneys. to study the behavior of the virus.
The results show extensive lung damage in most cases, with profound disruption of the normal lung structure and the conversion of respiratory tissue into fibrotic material.
Nearly 90% of patients exhibited two unique additional features of COVID-19 compared to other forms of pneumonia. Initially, the patients showed extensive blood clotting of the arteries and pulmonary veins (thrombosis). Second, several lung cells were unusually large and had many nuclei, which were the result of the fusion of several cells into single large cells. This fused cell formation (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 cause inflammation and thrombosis.
Furthermore, research has shown the long-term persistence of the virus genome in respiratory cells and the cells lining blood vessels, along with infected cellular syncytia. The presence of these infected cells can cause the greatest structural changes in the lungs, which can last for weeks or months and possibly explain the “long COVID”.
The study found no obvious signs of viral infection or persistent inflammation in other organs.
Professor Mauro Jacket of the British Heart Foundation Center at King’s College London said: “These results are very exciting. 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 persisting in the lungs for long periods of time. “
The team is now actively testing the effects of these abnormal cells on blood clotting and inflammation and looking for new drugs that can block the viral peak protein, causing the cells to fuse.
Reference: “The persistence of viral RNA, pneumocytic syncytia and thrombosis are hallmarks of advanced COVID-19 disease” by Rossana Bussani, Edoardo Schneider, Lorena Zentilin, Chiara Collesi, Hashim Ali, Luca Braga, Maria Concetta Volpe, Andrea Colliva and Fabrizio Zanconati. Giorgio Berlot and Furio Silvestri, 3 November 2020, eBioMedicine.
DOI: 10.1016 / j.ebiom.2020.103104.
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