COVID-19 Updates: Pathology Study Shows SARS-CoV-2 RNA Persistence, Pneumocyte Syncytia And Thrombosis In Human Host Lungs
: Pathology studies of deceased COVID-19 patients by researchers from King's College London in collaboration with the University of Trieste and the International Centre for Genetic Engineering and Biology in Italy have revealed that the human host lung damage is often characterized by SARS-CoV-2 viral RNA persistence, pneumocyte syncytia and thrombosis.
The study team reports the systematic analysis of 41 consecutive post-mortem samples from individuals who died of COVID-19. Histological analysis is complemented by immunohistochemistry for cellular and viral antigens and the detection of viral genomes by in situ RNA hybridization.
The findings showed that COVID-19 is characterized by extensive alveolar damage (41/41 of patients) and thrombosis of the lung micro- and macro-vasculature (29/41, 71%). Thrombi were in different stages of organization, consistent with their local origin. Pneumocytes and endothelial cells contained viral RNA even at the later stages of the disease. An additional feature was the common presence of a large number of dysmorphic pneumocytes, often forming syncytial elements (36/41, 87%). Despite occasional detection of virus-positive cells, no overt signs of viral infection were detected in other organs, which showed non-specific alterations.
The study findings were published in the Lancet's eBioMedicine
The investigations of deceased COVID-19 patients have shed light on possible lung damage caused by the virus and may explain why patients suffer from 'long COVID'.
Typically patients with COVID-19 can experience symptoms such as blood clotting and loss of smell and taste. Some who survive the infection can experience the effects of the disease for months - known as 'long COVID' - with a feeling of fatigue and lack of breath. There have been a limited number of studies that have analyzed the organs of COVID-19 patients which means the characteristics of the disease are still largely unknown.
The study team analyzed the organs of 41 patients who died of COVID-19 at the University Hospital of Trieste, Italy, from February to April 2020, at the start of the pandemic. The team took lung, heart, liver, and kidney samples to examine the behaviour of the virus.
Study findings showed extensive lung damage in most cases, with patients experiencing profound disruption of the normal lung structure and the transformation of respiratory tissue into fibrotic material.
Significantly almost 90% of patients showed two additional characteristics that were quite unique to COVID-19 compared to other forms of pneumonia. First, patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells.
This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells infected by the COVID-19 virus, it stimulates their fusion with other n
ormal lung cells, which can be a cause for inflammation and thrombosis.
Further detailed research showed the long-term persistence of the viral 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 observed in the lungs, which can persist for several weeks or months and could eventually explain 'long COVID'.
The research found no overt signs of viral infection or prolonged inflammation detected in other organs.
Dr Mauro Giacca, Professor, British Heart Foundation Centre, King's College London told Thailand Medical News, These study findings are very exciting. The findings indicate that COVID-19 is not simply a disease caused by the death of virus-infected cells but is likely the consequence of these abnormal cells persisting for long periods inside the lungs."
The study team is now actively testing the effect of these abnormal cells on blood clotting and inflammation and is searching for new drugs that can block the viral spike protein which causes cells to fuse.
The team concluded, “COVID-19 is a unique disease characterized by extensive lung thrombosis, long-term persistence of viral RNA in pneumocytes and endothelial cells, along with the presence of infected cell syncytia. Several of COVID-19 features might be consequent to the persistence of virus-infected cells for the duration of the disease.”
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