Long COVID-19 may be caused by abnormally suppressed immune system in some people: UCLA-led study
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A possible contributor to Long COVID -19 may actually be an abnormally suppressed, not overactive, immune system, according to a UCLA-led research group. The study, recently published in the peer-reviewed journal Clinical infectious diseases.
This contradicts what scientists previously believed, that an overactive immune response to SARS-CoV-2, often referred to as a “cytokine storm”, was at the root of the puzzled syndrome. Health experts told Fox News that this “cytokine storm” is a hyper-reactive inflammatory response in the infected person that can potentially damage the lungs and other organs, possibly leading to severe illness or even death.
Long COVID, which occurs in a subset of patients recovering from COVID-19, is a syndrome in which a multitude of symptoms, including shortness of breath, muscle aches, fatigue, voice fatigue, and brain fog , persist for several months after the acute infection stage, health experts told Fox News.
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According to the press release on the UCLA study, a limited understanding of the causes of long COVID makes treating the disease difficult.
“Although this is a small pilot study, it suggests that some people with long COVID may actually have an underactive immune system after recovering from COVID-19, which means that strengthening immunity in these people could be a treatment,” said Dr. Otto Yang, professor of medicine, division of infectious diseases and microbiology, immunology and molecular genetics at UCLA’s David Geffen School of Medicine, said. stated in a press release.
While investigating the notion that long COVID-19 is triggered by an underlying 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. Leronlimab is an antibody that binds to an immune receptor involved in inflammation called CCR5, the study authors explained in the release.
Participants were randomly selected to receive weekly injections of the antibody or a saline placebo for eight weeks. During that time, investigators tracked changes in 24 symptoms associated with long COVID, the statement said.
In the report, the investigators explained that they initially thought blocking CCR5 with Leronlimab would weaken the overactive immune system response after COVID-19 infection.
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“But we found the exact opposite,” Yang, who is also the lead author, said in the statement. “Patients who improved were those who started out with low CCR5 on their T cells, suggesting their immune system was less active than normal, and CCR5 levels actually increased in people who got better. This leads to the new hypothesis that the long COVID in some people is related to the fact that the immune system is suppressed and not overactive, and that while blocking its activity, the antibody can stabilize the expression of CCR5 at the cell surface, resulting in upregulation of other immune receptors or functions.
The researchers said in the statement that the results suggest “a complex role for CCR5 in balancing inflammatory and anti-inflammatory effects, for example via T regulatory cells.”
Dr. Aaron Glatt, a spokesperson for the Infectious Diseases Society of America, which was not affiliated with the study, commented on the results to Fox News and said, “This preliminary study presents intriguing new information regarding COVID-19 long-haul syndrome.” Glatt, who also serves as Chief of Infectious Diseases at Mount Sinai South Nassau Hospital on Long Island, New York, added: “At this point, however, our understanding of the pathogenesis of ‘long COVID’ remains unclear. further research to investigate a different potential mechanism.”
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The study authors said the findings need to be confirmed in a larger, more definitive study. The release also noted that the study was funded by Leronlimab manufacturer CytoDyn Inc. and conducted by researchers employed by or acting as consultants to the company.
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