COVID pneumonia is significantly different from pneumonia caused by other causes, new study reports. The infection leaves damage in its wake and fuels fever, low blood pressure, and damage to the kidneys, brain, heart and other organs in patients with COVID-19. Scientists have discovered a target for the treatment of COVID pneumonia.
The bacteria or viruses like the flu that cause pneumonia can spread to large areas of the lung over hours. In the modern intensive care unit, these bacteria or viruses are usually controlled either by antibiotics or by the body’s immune system in the first days of illness.
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The study published in the journal Nature, researchers at Northwestern Medicine show that COVID-19 pneumonia is different. Instead of rapidly infecting large areas of the lung, the virus that causes COVID-19 takes hold in several small areas of the lung. It then hijacks the lungs’ own immune cells and uses them to spread through the lungs over a period of days or even weeks, like multiple wildfires spreading through a forest.
As the infection slowly travels through the lungs it leaves damage in its wake and constantly fuels fever, low blood pressure, and damage to the kidneys, brain, heart, and others. organs in patients with COVID-19.
Serious complications of COVID-19 compared to other pneumonias could be linked to the long course of the disease rather than more serious illness, the study authors said.
This is the first study in which scientists have systematically analyzed immune cells in the lungs of patients with COVID-19 pneumonia and compared them with cells from patients with pneumonia due to other viruses or bacteria.
As a result of the detailed analysis, the researchers identified critical targets for treating severe SARS-CoV-2 pneumonia and reducing its damage. The targets are immune cells: macrophages and T cells. The study suggests that macrophage cells typically responsible for protecting the lungs can become infected with SARS-CoV-2 and may contribute to the spread of infection through lungs.
Northwestern Medicine will test an investigational drug to treat these targets in patients with COVID-19 pneumonia in a clinical trial in early 2021. The drug to be tested calms the inflammatory response of these immune cells, allowing the repair process to begin in the injured lung.
“Our goal is to make COVID-19 mild instead of severe, making it comparable to a bad cold,” said study co-author Dr Scott Budinger, chief of pulmonary medicine and critical care at Northwestern University Feinberg School of Medicine and Northwestern Medicine. .
COVID-19, like the flu, is unlikely to go away, even if a large part of the population is vaccinated, said lead co-author Dr Ben Singer, assistant professor of pulmonary medicine and intensive care at Feinberg and Northwestern Medicine physician.
“Researchers at Northwestern and elsewhere are already anticipating mechanisms by which this rapidly mutating RNA virus will escape current vaccines,” Singer said. The study also revealed why mortality among ventilator patients for COVID-19 was lower than ventilator patients due to regular pneumonia, the study reports. An intense conflagration in the lungs (regular pneumonia) has a higher risk of death.
People with COVID-19 pneumonia have been sick for a long time, but the inflammation in their lungs is not as bad as regular pneumonia.
“If patients with COVID-19 are carefully managed and the health care system is not overwhelmed, you can help them. These patients are very sick. It takes them a long time to get better. But if you have enough. beds and health care providers, you can keep mortality at 20%. When health systems are overwhelmed, death rates double to 40%, ”Budinger said.
For the study, scientists performed a high-resolution analysis of lung fluid from 86 COVID-19 patients on a ventilator and compared it to lung fluid from 256 patients on a ventilator who had other types of pneumonia. Due to safety concerns, only a handful of groups around the world have performed an analysis of the immune response in the lungs of patients with COVID-19.
The study at Northwestern Medicine is unique because Wunderink and his colleagues have been studying pneumonia for years before the pandemic. As a result, when the COVID-19 pandemic struck, they were ready to collect fluid from the lungs of these patients in a safe and systematic manner and compare it with fluid taken from other intensive care patients with pneumonia. collected before the pandemic. This research infrastructure has allowed them to show that pneumonia in COVID-19 patients is different from other pneumonias, and more importantly, how it is different.
Scientists took cells from the lung fluid of patients and examined the RNA and proteins expressed by these cells, allowing them to identify how these immune cells cause inflammation.
“This level of resolution could never be achieved without directly sampling lung fluid,” said study co-author Dr Alexander Misharin, assistant professor of pulmonary and intensive care medicine at Feinberg and physician at Northwestern. Medicine.
The complex nature of the study, in which patient samples were analyzed with the most sophisticated technologies available at Northwestern’s cutting-edge research laboratories, required the concerted effort of more than 100 researchers.
The first authors are Rogan Grant, Luisa Morales-Nebreda and Nikolay Markov. Grant is a graduate student of Northwestern University’s Interdepartmental Neuroscience Program; Dr Luisa Morales-Nebreda is a pulmonary and critical care researcher in Northwestern’s Physician Scientist Education Program; Nikolay Markovis is a postdoctoral researcher in informatics in the division of pulmonary medicine and intensive care.
The work was carried out as part of a consortium of investigators participating in the Center for Biology of Pneumonia Treatment Systems and Successful Clinical Response funded by the National Institute of Allergy and Infectious Diseases led by Wunderink.
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