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Covid-19 infections can unleash massive inflammation in the body

2022-04-07T03:45:01.645Z


A new study helps explain how these immune overreactions occur in COVID-19 patients. Psychological effects of prolonged covid-19 5:16 (CNN) — From the earliest days of the pandemic, doctors have noted that in severe cases of Covid-19, the ones that landed hospitalized people on ventilators with their lungs lacerated, most of the internal damage was unprovoked. directly by the virus, but by a wave of immune reactions of the body itself to fight the infection. The researchers knew


Psychological effects of prolonged covid-19 5:16

(CNN) —

From the earliest days of the pandemic, doctors have noted that in severe cases of Covid-19, the ones that landed hospitalized people on ventilators with their lungs lacerated, most of the internal damage was unprovoked. directly by the virus, but by a wave of immune reactions of the body itself to fight the infection.

The researchers knew that these so-called cytokine storms were harmful, but not why the SARS-CoV-2 virus seemed so efficient at triggering them.

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

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 part of the front line of the immune system.

Their job is to circulate in the blood and tissues, to find and destroy pathogens.

They do this by gobbling up, or rather surrounding and absorbing, threats like viruses to prevent them from infecting other cells.

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Once a harmful element is absorbed, these cells have what could be described as a cellular garbage disposal, called an endosome, which normally deactivates the infectious agent.

However, in the case of the SARS-CoV-2 virus, that does not happen.

The virus breaks out of the endosome and escapes into the cell body, where it begins to make copies of itself.

"Viruses are not just absorbed, but then the virus starts to replicate, which is amazing," said Dr. Judith Lieberman, a pediatric immunologist at Boston Children's Hospital, who led the research.

A virus starting to make copies of itself in the body is never a good thing, but when it happens to these protective cells, it sets off a next-level set of alarm bells.

an inflamed death

These alarms, in turn, summon agents called inflammasomes, which essentially respond by burning everything.

They help the infected cell to die by pyroptosis or "burning death".

Pyroptosis is a recently recognized phenomenon.

It occurs in other diseases as well, such as sepsis.

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"When cells die from pyroptosis, they release all sorts of inflammatory proteins that cause fever and call more immune cells to the site," Lieberman said.

It triggers a cascade of crisis signals that is very difficult to stop.

“We have no way of dealing with that once it starts.

It's like a small fire.

It spreads and explodes, and no fire extinguisher is capable of putting it out,” he said.

"I think it's really elegant," said Donna Farber, a professor of microbiology and immunology at Columbia University, describing the study.

"They actually put together some pieces that hadn't been put together before."

She was not involved in the investigation.

By comparing blood cells from healthy people with those from people who came to the hospital with COVID-19, and with blood from people who had pneumonia from other causes, the researchers found that this process appears to occur more often with COVID-19.

"All the patients we studied had signs of respiratory distress and pneumonia. The ones with [SARS-CoV-2] had a lot more of these inflammasomes and dying cells," Lieberman said.

"So it's likely that [SARS-CoV-2] is particularly effective at inducing it, but we don't know why."

Lieberman said the study also helps explain why older people or those with underlying health conditions, such as obesity or diabetes, are at higher risk for serious outcomes with Covid-19.

Those conditions are already associated with some level of inflammation in the body.

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"It's much, much more likely that these inflammatory fires will start in them," he said.

"Anyway, they have kind of a slow burn down. And once it starts, it's really hard to put the fire out."

The role of antibodies

However, there is another part of the process that suggests a way to stop it, and that is the way the virus enters white blood cells.

Monocytes and macrophages do not have ACE-2 receptors, the gates that the virus uses to attach to and infect other types of cells.

Instead, the virus enters these cells due to another immune system helper: Y-shaped antibodies that latch onto the virus in an attempt to prevent it from attaching to our cells.

When antibodies catch viruses, the tail of the antibody, called the FC portion, sticks out.

That stalk acts as a signal to monocytes and macrophages to let them know there's a bad guy to catch.

Not all monocytes recognize the same antibodies.

The study found that people with COVID-19 tended to have more than one unusual type of monocyte that had CD16 receptors.

These receptors recognize the antibody stems that the body produces to fight the SARS-CoV-2 virus.

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Those antibodies connect to monocytes with CD16 receptors, causing the cell to take up the virus.

Once inside, the virus starts trying to copy itself, triggering the damaging inflammatory reaction.

John Wherry, director of the Institute of Immunology at the Perelman School of Medicine at the University of Pennsylvania, said that's something they've been wondering about with Covid-19 infections, if there might be some kind of increased disease antibody. .

Wherry was not involved in the study.

He said this can also happen with other infections, such as dengue fever.

The more times a person is infected with the dengue virus, the sicker they become with each new attack.

It is the opposite of what is supposed to happen.

A person who recovers from an infection is usually better protected against future infections.

Pharmacological targets

Wherry said there is no evidence that the antibodies that facilitate these severe inflammatory reactions come from previous infections or from other types of coronavirus.

He said that antibodies are produced rapidly in infections and that the ones at work here were probably produced in response to the person's current illness.

Different from what happens with dengue.

However, the antibodies generated by the vaccines do not seem to facilitate monocyte infections and their inflammatory cascades.

They did tests in the studio.

"I think what's interesting about this is that it could provide a clue and maybe even some drug targets for why some of the inflammation that we see in severe COVID patients may start to get worse or get out of control," Wherry said.

"So that's where I think this is quite interesting."

Covid-19

Source: cnnespanol

All news articles on 2022-04-07

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