PARIS, April 6 (Benin News) –
A study by researchers at Boston Children’s Hospital (USA) has explained for the first time why COVID-19 causes severe inflammation in some people, leading to acute respiratory distress and multiple organ damage.
Surprisingly, the study, published in the scientific journal Nature, also reveals that antibodies developed by people who contract COVID-19 can sometimes cause more inflammation, while antibodies generated by mRNA vaccines of COVID-19 do not seem to do so.
“We wanted to understand what distinguishes patients with mild and severe COVID-19. We know that many inflammatory markers are elevated in people with severe disease, and that inflammation drives disease severity, but we didn’t know what triggers inflammation,” says Judy Lieberman, study manager.
The researchers analyzed fresh blood samples from patients with COVID-19 who presented to the emergency department at Massachusetts General Hospital. They compared them to samples from healthy people and patients with other respiratory conditions. They also examined lung autopsy tissue from people who died of COVID-19.
They found that SARS-CoV-2 can infect monocytes (immune cells in the blood that act as “sentinels” or first responders to infection) as well as macrophages, similar immune cells found in the lungs. Once infected, both cell types undergo a violent death (called pyroptosis) which releases a burst of powerful inflammatory warning signals.
“In infected patients, approximately 6% of blood monocytes died an inflammatory death. This is a significant number, because dying cells are rapidly eliminated from the body,” says Lieberman.
When they examined lung tissue from people who had died from COVID-19, they found that about a quarter of the macrophages in the tissue were dying.
When the researchers studied the cells for signs of SARS-CoV-2, they found that about 10% of monocytes and 8% of lung macrophages were infected.
The fact that monocytes and macrophages can be infected with SARS-CoV-2 came as a surprise, as monocytes do not carry ACE2 receptors, the virus’ classic entry gate, and macrophages have low amounts of ACE2 receptors. ‘ACE2.
Lieberman thinks SARS-CoV-2 infection of monocytes may have gone unnoticed in part because researchers often study frozen blood samples, in which dead cells do not appear.
The study also showed that while SARS-CoV-2 was able to infect monocytes and macrophages, it was unable to produce infectious new virus. The researchers believe the cells were quickly killed by pyroptosis before the new viruses could fully form.
In a sense, the uptake of the virus by these “sentinel” cells is protective: it absorbs the virus and recruits other immune cells. But the bad news is that all those inflammatory molecules are released. In people who are more prone to inflammation, like older people, it can get out of control,” adds Lieberman.