Bacteria or viruses like influenza that cause pneumonia can spread across large regions of the lung over the course of hours.
In the modern intensive care unit, these bacteria or viruses are usually controlled either by antibiotics or by the body’s immune system within the first few days of the illness.
But in a new study, researchers found COVID-19 pneumonia is different.
Instead of rapidly infecting large regions of the lung, the virus causing COVID-19 sets up shop in multiple small areas of the lungs.
It then hijacks the lungs’ own immune cells and uses them to spread across the lung over a period of many days or even weeks, like multiple wildfires spreading across a forest.
As the infection slowly moves across the lung, it leaves damage in its wake and continuously fuels the fever, low blood pressure, and damage to the kidneys, brain, heart, and other organs in patients with COVID-19.
The researchers say that the severe complications of COVID-19 compared with other types of pneumonia might be related to the long course of the disease rather than more severe disease.
The research was conducted by a team at Northwestern Medicine.
In the study, the team identified critical targets to treat severe SARS-CoV-2 pneumonia and lessen its damage. The targets are the immune cells: macrophages and T cells.
The study suggests macrophages—cells typically charged with protecting the lung—can be infected by SARS-CoV-2 and can contribute to spreading the infection through the lung.
Northwestern Medicine will test an experimental drug to treat these targets in COVID-19 pneumonia patients in a clinical trial early in 2021.
The drug to be tested quiets the inflammatory response of these immune cells, thus enabling initiation of the repair process in the injured lung.
The goal is to make COVID-19 mild instead of severe, making it comparable to a bad cold.
One author of the study is Dr. Scott Budinger, the chief of pulmonary and critical care medicine.
The study is published in Nature.
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