Bacteria or viruses that cause pneumonia can spread across large regions of the lung within hours. But Covid-19 pneumonia is different, researchers at Northwestern University Medicine explain in a new study published in the journal Nature.
In pneumonia caused by bacteria and viruses like influenza, these agents can usually be controlled by antibiotics, or by the body’s immune system, within the first few days of the illness. The virus responsible for Covid-19, however, does not rapidly infecting large regions of the lung like other viruses. Instead, SARS-CoV-2 sets up shop in multiple small areas of the lung, the study has found. The virus 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”, Northwestern University said in a statement on the research.
And 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 severe complications of Covid-19 compared with other pneumonias might be related to the long course of disease rather than more severe disease, the study authors said.
According to Northwestern University, this is the first study in which scientists analysed immune cells from the lungs of Covid-19 pneumonia patients in a systematic manner and compared them to cells from patients with pneumonia from other viruses or bacteria.
As a result of the detailed analysis, researchers 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 that 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 university said.
“Our goal is to make Covid-19 mild instead of severe, making it comparable to a bad cold,” Northwestern quoted study co-senior author Dr Scott Budinger as saying. And co-senior author Dr Richard Wunderink was quoted as saying: “This effort truly represents a ‘moonshot’ in Covid-19 research.”
The study also found reasons why the mortality among patients on a ventilator for Covid-19 was lower than patients on a ventilator due to regular pneumonia. An intense conflagration in the lungs (regular pneumonia) has a higher risk of death. Those with Covid-19 pneumonia are sick for a long time, but the inflammation in their lungs is not as severe as regular pneumonia.
Source: Northwestern University