The bacteria or viruses like the flu that cause pneumonia can spread over large areas of the lung over the course of hours. In an intensive care unit (ICU), these bacteria or viruses are controlled by antibiotics or by the immune system during the first days of the illness.
But according to a study published in “Nature”, COVID-19 pneumonia is different.
Rather than rapidly infecting large regions of the lung, the virus that causes COVID-19 settles in multiple small areas of the lung. It then hijacks the lungs’ own immune cells and uses them to spread through the lung for an extended period of time, days or even weeks, like multiple wildfires raging through a forest. And, as the infection moves slowly through the lung, it leaves damage in its wake and continually fuels fever, and damage to the kidneys, brain, heart, and other organs.
“It is a totally different mechanism,” says Germán Peces Barba, from the Jiménez Díaz Foundation University Hospital and group leader at CIBERES.
“In a sibylline way -says the pulmonologist Rosario Menéndez- it creates foci in the lung that, little by little they are distributed and causing the injury”. This expert from the Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) explains that this dissemination of foci produces a «amplifying effect of the inflammatory response that can sometimes lead to so-called respiratory distress which, in the worst case, will require oxygen and mechanical ventilation».
And this ‘different’ mechanism of action, adds Peces Barba, means that this entity has a different prognosis and that some drugs will not work. But, curiously, says Peces Barba, “the mortality of cases of pneumonia due to covid-19 is lower than that of conventional pneumonia.”
Thus, the study shows that mortality among patients on mechanical ventilation due to Covid-19 was lower than that of ventilated patients with regular pneumonia. “People with covid-19 pneumonia are sick for a long time, but the inflammation of the lungs is not as severe as normal pneumonia.”
The severe complications of COVID-19 compared to other pneumonias could be related to the prolonged course of the disease rather than a more serious illness, the study authors say.
The study is very relevant, highlights Dr. Menéndez, a pulmonologist at Hospital La Fe (Valencia), because it is one of the first in which the immune cells of the lungs of patients with COVID-19 pneumonia have been systematically obtained from through bronchoalvelar lavage and compared with cells from patients with pneumonia from other viruses or bacteria.
Specifically, he explains, “they have seen that macrophages – cells of the immune system – are not capable of fighting the virus that uses these cells to live inside and uses it as a ‘trojan‘”. In this way, “the virus spreads throughout the lung generating different foci, visible through imaging tests.”
The data from this work, says the SEPAR pulmonologist, supports the hypothesis that the inflammation and damage persists longer than conventional pneumonia. And that damage, he warns «affects other organs, such as the endothelium -inner layer of blood vessels- and endothelitis -inflammation of the endothelium-, would explain the long-term damage of the disease».
An added problem, the CIBERES pulmonologist points out, is that «we do not have early detection systems or markers to determine which patients with pneumonia are going to get worse, there is no common pattern, and in a few hours they can be complicated.
Fortunately, there are treatments, Menendez points out, “because we have learned over time what works – corticosteroids, remdesivir … – and what does not work – antivirals, hydroxychloroquine … -“. But, he stresses, “we would like to have more antivirals. We have more antibacterials than antivirals.
In the study of «Nature»Researchers have also identified critical new targets for treating severe SARS-CoV-2 pneumonia and reducing its harm. These targets, they write, would be immune cells: macrophages and T cells.We have seen that macrophages, cells in charge of protecting the lung, can become infected with SARS-CoV-2 and help spread the infection through the lung».
For this reason, researchers at Northwestern Medicine University (USA) are testing an experimental drug targeting these targets in patients with COVID-19 pneumonia in an ongoing clinical trial. “The drug inactivates the inflammatory response of these immune cells, which allows the start of the repair process in the injured lung,” they detail in their article.
“Our goal is to turn COVID-19 into a mild illness, comparable to a severe cold,” says study co-author Scott Budinger.
The information in this work is relevant because, according to this team, «this rapidly mutating RNA virus will elude current vaccines», Hence the importance of developing treatments to reduce the severity of covid-19 in those who develop it