How a COVID-19 infection tricks your body into attacking yourself

From the early days of the pandemic, doctors Severe cases of COVID-19 -What landed people Ventilator hospital In the shredded lungs-most of the internal debris was not caused directly by the virus itself, but by a snowstorm of an immune response caused by the body to fight the infection.

The researcher knew They did not know that these so-called cytokine storms were harmful, but they did not know why the SARS-CoV-2 virus appeared to be very good at causing them.

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A new study published in the journal on Wednesday Nature It helps explain how these immune overreactions occur in patients with COVID-19.

The study revealed that the SARS-CoV-2 virus can infect certain types of immune cells called monocytes and macrophages.

Frontline immune cells are infected

Monocytes and macrophages are white blood cells and are the frontline workers of the immune system. Their job is to circulate blood and tissues to find and destroy pathogens. They do this by eating, actually surrounding, and absorbing virus-like threats to prevent them from infecting other cells.

When a malicious person is absorbed, these cells have what is best described as cell waste disposal, called endosomes, and usually shut down infectious pathogens.

But with the SARS-CoV-2 virus, that doesn’t happen. The virus exits the endosome and escapes into the cell body, where it begins to make its own copy.

Dr. Judith Leiberman, a pediatric immunoscientist at Boston Children’s Hospital, who led the study, said:

It’s never a good thing for the virus to start making copies of itself in the body, but when this happens to these protector cells, it triggers the next set of alarms.

Fiery death

These alarms call an agent called the inflammasome. The inflammasome responds by burning everything in essence. They help infected cells die by pyroposis, or “burning death.”

Pyroptosis is a newly recognized phenomenon. It also happens with other illnesses like sepsis.

“When cells die from pyroptosis, they release all sorts of inflammatory proteins that cause fever, evoking more immune cells at the site,” Lieberman said. It causes a cascade of crisis signals that is very difficult to stop.

“Once you start, there’s no way to handle it. It’s like a little fire. It spreads, explodes, and the fire extinguisher can’t put it out,” she said.

“I think it’s really elegant,” explained Donna Farber, a professor of microbiology and immunology at Columbia University. “They actually assembled some parts that weren’t previously assembled.” She wasn’t involved in the study.

Comparing the blood cells of healthy people with those of people hospitalized with COVID-19 and those of people with pneumonia for other reasons, researchers find that this process appears to occur more frequently with COVID-19. discovered.

“All the patients we studied had signs of dyspnea and pneumonia. Those who had (SARS-CoV-2) had more of these inflammasomes and dying cells. “It was,” said Lieberman. “Therefore, (SARS-CoV-2) may be particularly good at inducing it, but I don’t know why.”

According to Lieberman, the study also helps explain why elderly people and people with underlying health problems such as obesity and diabetes are at increased risk of serious outcomes from COVID-19. I did. These conditions are already associated with some inflammation in the body.

“They are much more likely to cause these inflammatory fires,” she said. “Anyway, they’re experiencing some sort of slow burning, and once started, it’s really hard to put out the fire.”

Role of antibody

But there is another part of the process. It suggests a way to stop it, which is how the virus invades these white blood cells.

Monocytes and macrophages do not have ACE-2 receptors. This is the door that the virus uses to dock and infect other types of cells. Instead, the virus invades these cells for another immune system helper, a Y-shaped antibody that grabs the virus in an attempt to stop it from docking to the cells.

When the antibody grabs the virus, the tail of the antibody, called the FC part, sticks out. Its stem acts as a flag to swing down monocytes and macrophages to signal that there is a bad guy to pick up.

Not all monocytes recognize the same antibody. This study found that people with COVID-19 tend to have a rare type of monocyte with the CD16 receptor. These receptors recognize the stems of antibodies that the body makes to fight the SARS-CoV-2 virus.

These antibodies connect to monocytes at the CD16 receptor and trigger the cells to absorb the virus. Once inside, the virus begins trying to copy itself, causing a harmful inflammatory reaction.

John Wellie, director of the Institute of Immunology at the University of Pennsylvania’s Perelman School of Medicine, said that we suspected that some antibodies might enhance the disease for COVID-19 infections. I did. Wherry was not involved in the study.

He said this could also happen with other infections like dengue. The more a person becomes infected with the dengue virus, the more ill he gets with each subsequent attack. It’s the opposite of what’s supposed to happen. People who have recovered from an infection usually have better protection against future infections.

Drug discovery target

Welly said there was no evidence that the antibodies that promote these severe inflammatory responses were derived from previous infections or other types of coronavirus. He said the antibodies were made quickly with an infection, and the ones working here were probably made according to the person’s current illness. As such, it is different from what happens with dengue fever.

However, the antibodies produced by the vaccine do not appear to promote monocyte infection and the subsequent inflammatory cascade. They tested it in a study.

“What’s interesting about this is that it provides clues as to why some of the inflammation seen in severely ill COVID patients kickstarts in the wrong way or progresses out of control, and perhaps some drug targets. I think we can do it, “says Wheely. .. “So I think this is very interesting.”