New research has revealed that fragments of the “zombie” coronavirus still linger for some, causing serious illness outcomes

New research has revealed that fragments of the “zombie” coronavirus still linger for some, causing serious illness outcomes

Although the COVID-19 pandemic has largely faded from the public’s mind, the infection is still very common and not always as benign as influenza. There is a link betweenInflammation, the immune system and COVID-19 are not yet fully understood and could cause thousands of deaths and disabilities.

As Salon previously reported, severe cases of the coronavirus can trigger an excessive inflammatory response called a “cytokine storm” so severe that it appears to deplete T cells important for immune function and reduce their number. There has been evidence to suggest that this could affect the immune system’s ability to fight future infections caused by Covid-19 and other diseases as well. More recently, researchers found that inflammation caused by COVID-19 in pregnant women triggered an inflammatory response in their infants, causing respiratory distress after birth.

There’s something specific about infection with SARS-CoV-2, the virus that causes COVID-19, and how it can sometimes trigger an overactive immune response. However, how this happens remains a mystery.

But now, researchers at the University of California-Los Angeles say they are one step closer to understanding how COVID-19 can sometimes lead to serious outcomes or death, while other coronaviruses like the common cold do not. They believe the answer lies in so-called “zombie” virus fragments that remain and cause inflammation long after the virus is destroyed.

“After destroying this virus that should be dead, it is not.”

“There’s a kind of biomimicry that’s going on here, that once the virus degrades, these pieces actually become active and can assemble with the dsRNA that’s normally found in viral infections,” says Gerard Wong, corresponding author and professor of microbiology. an immunologist and molecular geneticist at the University of California-Los Angeles, told Salon in an interview. “And that’s the part about zombies – after you destroy this virus that’s supposed to die, it’s not. In fact, it can reassemble into these complexes that can have a very strong immune activation capacity.”

As Wong noted, once the virus interacts with the human immune system, the virus usually divides to a point where the host and its immune system win. As a result, the immune system learns from this interaction and builds immunity to that virus by knowing exactly how to defeat it next time. But it doesn’t work quite that way with SARS-CoV-2.


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As described in their study that will be published in the journal According to this week’s Proceedings of the National Academy of Sciences, a coronavirus (COVID-19) infection can turn the immune system against the body with disastrous and sometimes fatal outcomes — a pattern that deviates from the standard course of viral infections and what scientists expect to happen. See immunology.

This suggests that more severe COVID-19 outcomes are a result of these residual fragments essentially over-stimulating the immune system.

To find this strange pattern with COVID-19 infection, Wong and his colleagues developed an artificial intelligence system to scan a set of proteins produced by SARS-CoV-2 infection. After the examination, they conducted a series of validation experiments, some of which used mice. By combining the two methods, the researchers found that specific viral fragments remaining from SARS-CoV-2 infection break down into fragments and mimic immunogenic peptides responsible for exacerbating immune responses. This suggests that more severe COVID-19 outcomes are a result of these residual fragments essentially over-stimulating the immune system. As a result, this causes rampant inflammation in some people.

Wong compared it to eating five croissants from a bakery. Once croissants are digested, their effect is no longer as well, and they can negatively affect cardiovascular health, for example. Of course, this does not happen all the time with every Covid-19 infection. For some people, the infection is mild and symptoms do not last long. But for others, it can lead to long Covid, where symptoms last for months or never go away. Wong said the reason why splinters persist and cause severe inflammation in some people and not others could be due to a difference in enzymatic activity, which is the way proteins are broken down in the human body, which varies from person to person.

“I think the fact that there is such heterogeneous enzymatic activity between different hosts is one of the reasons why someone can sometimes be unlucky enough to get the wrong part in the wrong place at the wrong time,” he said. “And that could mediate a lot of these types of effects.”

This is the first of several papers that will look in depth at this specific interaction and its potential consequences, Wong said. In the long term, he hopes this will help build a surveillance system that can help distinguish between harmful strains of the SARS-CoV-2 virus and those that are less dangerous based on how “molecular models” amplify the immune response. He also hopes this will lead to better treatment opportunities for Covid-19. Currently, severe cases can be treated with antiviral medications such as baxlovid.

“Maybe what needs to be done is to find ways to take up the viral fragments, assemble them into a non-inflammatory form, and be able to force this shift in the immune system,” he said. “So we don’t get all these results.”

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