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SARS-CoV-2 causes severe inflammation in some people. Method is as follows.

SARS-CoV-2 causes severe inflammation in some people. Method is as follows.


Severe COVID-19 infections are known to be associated with increased inflammation. However, it is not understood how SARS-CoV-2 causes inflammation. Researchers are now showing for the first time how COVID-19 causes severe inflammation in some people, causing acute respiratory distress and multiple organ failure.

This study found that SARS-CoV-2 can infect monocytes and macrophages. Upon infection, both types of immune cells die via pyroptosis and emit an explosion of inflammatory alarm signals. Surprisingly, in this study, antibodies developed by people with COVID-19 may cause more inflammation, but antibodies produced by the mRNA COVID-19 vaccine do not appear to be.

This work is published in NatureIn the article, “Monocyte FcγR-mediated SARS-CoV-2 infection activates inflammation.

Investigators analyzed fresh blood samples from COVID-19 patients in the emergency department of Massachusetts General Hospital in Boston. They compared these with samples from healthy people and patients with other respiratory illnesses. They also examined the lung autopsy tissue of people who died of COVID-19.

Judy Lieberman, MD, professor of pediatrics at Harvard Medical School, said: “We know that many inflammation markers are elevated in people with severe illness and that inflammation is at the root of the severity of the illness, but we did not know what causes it.”

They discovered that SARS-CoV-2 can infect monocytes (immune cells in the blood) and macrophages (in the lungs). The authors explain that both monocytes and macrophages are sentinel cells that form the inflammasome that senses invasive infections and activates caspase-1 and gasdermin D. This results in inflammatory death known as pyroptosis and the release of potent inflammatory mediators.

Researchers have found that about 6% of blood monocytes in COVID-19 patients are infected with SARS-CoV-2. “In infected patients, about 6% of monocytes in the blood resulted in inflammatory death,” said Lieberman. “It’s a very large number to find, as dying cells are rapidly eliminated from the body.”

Examination of the lung tissue of people who died of COVID-19 revealed that about a quarter of the macrophages in the tissue were dead. When researchers studied 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 infect SARS-CoV-2 is surprising because monocytes do not have the ACE2 receptor, which is the classic entry portal for the virus, and the amount of ACE2 in macrophages is low. was. Lieberman believes that monocyte SARS-CoV-2 infections may have been previously overlooked, as researchers often study frozen blood samples that do not show dead cells. ..

The study also showed that SARS-CoV-2 was able to infect monocytes and macrophages, but not to produce new infectious viruses. Researchers believe that cells died rapidly from pyroptosis before the new virus was completely formed.

“In a sense, the uptake of the virus by these” sentinel “cells is protective. It absorbs the virus and mobilizes more immune cells, “Rieberman said. “But the bad news is that all these inflammatory molecules are released. In people who are prone to inflammation, such as the elderly, this can go out of control.”

Certain groups of monocytes, namely those with the CD16 receptor, were particularly susceptible to infection. These “non-classical” monocytes make up only about 10% of all monocytes, but their numbers are increasing in patients with COVID-19. In addition, it is more likely to be infected, and about half of them were infected compared to the case without conventional blood monocytes.

The CD16 receptor recognizes antibodies to the SARS-CoV-2 spike protein. Researchers believe that these antibodies may promote the infection of receptor-carrying monocytes. “Antibodies cover the virus and cells with CD16 receptors take up the virus,” says Lieberman.

However, when the team studied healthy patients vaccinated with the mRNA vaccine against COVID-19, the antibodies they developed did not appear to promote infection. The reason for this is still unknown. Researchers suggest that vaccine-generated antibodies have slightly different properties than antibodies that occur during infection and do not also bind to the CD16 receptor. As a result, the cells do not absorb the virus.

Lieberman and her colleagues believe that these findings may affect the use of monoclonal antibodies in the treatment of COVID-19, and why they are only effective if treatment is given early. Helps to explain. “Later, it may be that the antibody may help increase inflammation,” she says. “It may be necessary to examine the properties of the antibody.”




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