Long-term cause of COVID-19 may be an abnormally suppressed immune system in some people: UCLA-led study

A potential contributor to COVID-19 may actually be an abnormally suppressed immune system, rather than an overactive system, according to a research group led by UCLA. The study was recently published in the peer-reviewed journal Clinical infectious diseases.

It contradicts what scientists previously believed, which is that an excessive immune response to SARS-CoV-2, often referred to as a “cytokine storm,” was the root cause of the bewilderment syndrome. Health experts told Fox News that this “cytokine storm” is an overreactive inflammatory response in an infected person that can cause damage to the lungs and other organs, possibly causing severe illness or even death.

COVID prolongation, which occurs in a subset of patients who recover from COVID-19, is a syndrome where many symptoms including shortness of breath, muscle aches, fatigue, vocal fatigue and brain fog persist for months after the acute infection phase, health experts explained to Fox News.

The study suggests that time-restricted eating is no more beneficial than calorie restriction in obese patients.

According to the press release about the UCLA study, limited understanding of the longstanding causes of COVID makes treating the condition difficult.

“Although this was a small pilot study, it does suggest that some people who have had COVID for a long time may actually have an underactive immune system after recovering from COVID-19, which means that boosting immunity in these individuals could potentially help. be a cure,” said Dr. Otto Yang, MD, professor of medicine, division of infectious diseases, microbiology, immunology and molecular genetics at UCLA’s David Geffen School of Medicine in a press release.

يتم اختبار امرأة في شاحنة اختبار COVID-19 متنقلة <span class ="حقوق النشر"> Liao Pan / China News Service via Getty Images </span>” data-src=”https://s.yimg.com/ny/api/res/1.2/BaQb.ACBaI0hp5K9GgUC.w–/YXBwaWQ9aGlnaGxhbmRlcjt3PTcwNTtoPTM5Nw–/https://s.yimg.com/uu/api/ res/1.2/fc6plYw4sFLhsytvh3WuUQ–~B/aD03MjA7dz0xMjgwO2FwcGlkPXl0YWNoeW9u/https://media.zenfs.com/en/fox_news_text_979/720c720c5b061794b52d8>fd8<noscript><img alt= Liao Pan / China News Service via Getty Images ” src=”https://s.yimg.com/ny/api/res/1.2/BaQb.ACBaI0hp5K9GgUC.w–/YXBwaWQ9aGlnaGxhbmRlcjt3PTcwNTtoPTM5Nw–/https://s.yimg.com/uu/api/res/ 1.2/fc6plYw4sFLhsytvh3WuUQ–~B/aD03MjA7dz0xMjgwO2FwcGlkPXl0YWNoeW9u/https://media.zenfs.com/en/fox_news_text_979/720c720c5b4374b52d80d8dasb94a>”classimg”

A woman being tested in a mobile truck for COVID-19 testing Liao Pan / China News Service via Getty Images

While investigating the idea that prolonged COVID-19 is caused by an overactive immune response, the UCLA-led team of researchers studied the effect of the monoclonal antibody Leronlimab on Long COVID-19, in a small exploratory trial involving 55 people with the condition. In the statement, the study authors explained that Leronlimab is an antibody that binds to an immune receptor implicated in inflammation called CCR5.

Participants were randomly assigned to receive weekly injections of either the antibody or a saline placebo for eight weeks. During that period, investigators tracked changes in 24 symptoms associated with prolonged COVID, according to the statement.

In the report, the investigators explained that they initially believed that blocking CCR5 with Leronlimab would impair the response of an overactive immune system after a COVID-19 infection.

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“But we found just the opposite,” Yang, who is also the lead author, said in the statement. “The patients who improved were those who started with a low level of CCR5 on their T cells, indicating that their immune system was less active than usual, and that CCR5 levels actually increased in people who improved. This leads to a new hypothesis that COVID is prolonged in the Some people relate to the immune system being suppressed rather than overactive, and that while inhibiting its activity, the antibody can stabilize CCR5 expression on the cell surface leading to the upregulation of receptors or other immune functions.”

In the statement, the researchers stated that the findings suggested “a complex role for CCR5 in balancing inflammatory and anti-inflammatory effects, for example through regulatory T cells.”

Dr. Aaron Glatt, a spokesperson for the Infectious Diseases Society of America, who was not affiliated with the study, commented on the findings to Fox News and said, “This preliminary study provides interesting new information regarding the long-term COVID-19 syndrome.” He is also the chief of infectious diseases at Mount Sinai South Nassau Hospital on Long Island, New York,” At this time, however, our understanding of the pathogenesis of ‘long COVID’ remains unclear. This study supports further research to investigate a different potential mechanism .”

The study authors stated that the findings need to be confirmed in a larger, more specific study. Also noted in the release, the study was funded by CytoDyn Inc.’s manufacturer Leronlimab. It was conducted by researchers who either act or act as advisors to the company.

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