An international team led by DZL researcher Dr. Danny Jonigk has been able to prove changes in the lung tissue caused by SARS-CoV-2. The findings of the study show a funda-mental difference to lung damage caused by influenza viruses.
An infection with the coronavirus, just like a severe flu, may severely damage the respiratory tract and lead to fatal respiratory failure. So far, however, hardly anything is known about which molecular changes SARS-CoV-2 triggers precisely in the lung tissue of patients and how these differ from damage caused by the influenza virus. In order to obtain a better understanding of the disease processes, an international team of researchers from Germany, the U.S., Belgium, and Switzerland led by DZL professor Dr. Danny Jonigk, lung specialist at the Institute for Pathology of Hannover Medical School (MHH), has now examined the lungs of people who died from COVID-19 and compared them with those who died from the flu (influenza). “The study improves our understanding of as to why lung function is so significantly impaired in people infected with SARS-CoV-2 who have a severe course of the disease“, Professor Jonigk points out. The findings of the study titled “Pulmonary Vascular Endothelialitis, Thrombosis and Angiogenesis in COVID-19” have now been published in the renowned medical journal New England Journal of Medicine.
“For the first time, we have examined tissue samples synergistically using a very wide range of methods including micro-computed tomography, 3D electron microscopes and various molecular biological methods in order to track the pathways of SARS-CoV-2,“ professor Jonigk states. Here, the scientist have initially been able to show the already known acute damage pattern in the lungs of COVID-19 patients, also referred to as diffuse alveolar damage, which occurs when the walls of the alveoli become inflamed, are extensively covered by protein deposits, thus reducing oxygen supply to the blood. “We also found a massive number of blood clots in all sections of the blood vessels in the lungs, but particularly in capillaries, the thinnest vessels,” the pathologist states. “These microthrombi block thin pulmonary vessels and contribute to increased dyspnea in the patient.” Although this phenomenon can also be observed in lungs severely damaged by influenza infections, the amount of such small blockages is significantly smaller in people who died from the flu.
There’s another finding physicians predominantly only see in tumor diseases, autoimmune diseases or scarring processes: SARS-CoV-2 apparently triggers a special type of new vessel formation in the lungs. “This intussusceptive neoangiogenesis, as it is called, has not yet been described in the context of diffuse alveolar damage and fundamentally differentiates Covid-19 from lung infections caused by influenza viruses that are of comparable severity,“ Professor Jonigk points out and then summarizes: “The three changes in the lungs occurring in SARS-CoV-2 infections that have comprehensively been described in our study for the first time include massive damage to blood vessels, excessive blood clotting with blocking of the thinnest lung vessels, and the formation of new blood vessels, which is characteristic of COVID-19.“
The pathologist regards the findings of the study as another piece of the puzzle when it comes to decoding COVID-19. However, the coronavirus conundrum is far from being solved. Further studies are required to understand the mechanisms of changes in the vessels and eventually apply them in therapeutic approaches.
Professor Dr. Danny Jonigk
AG-Lungenforschung@mh-hannover.de
Maximilian Ackermann, M.D., Stijn E. Verleden, Ph.D., Mark Kuehnel, Ph.D., Axel Haverich, M.D., Tobias Welte, M.D., Florian Laenger, M.D., Arno Vanstapel, Ph.D., Christopher Werlein, M.D., Helge Stark, Ph.D., Alexandar Tzankov, M.D., William W. Li, M.D., Vincent W. Li, M.D., Steven J. Mentzer, M.D., and Danny Jonigk, M.D., et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. New England Journal of Medicine. DOI: 10.1056/NEJMoa2015432
Source: idw
