Breakthrough discovery might reveal what causes Long COVID
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- Researchers from Yale might have discovered why some of the patients infected with the novel coronavirus develop severe forms of COVID-19.
- They found that patients with severe COVID-19 developed autoantibodies that attacked healthy cells instead of the virus, including interferon and B and T cells, thus hindering the immune response to the infection.
- The researchers speculate that this autoimmune response might favor Long COVID.
- If the hypothesis is correct, doctors will be able to formulate new therapies to treat patients experiencing long-term effects of the virus.
The more time passes, the more COVID-19 mysteries can be explained. Now, a team of Yale researchers might have just delivered what appears to be another breakthrough discovery. If their hypothesis is accurate, then the scientists might have provided the first explanation for Long COVID, the chronic type of coronavirus-like illness that follows the infection in some patients. This team of researchers discovered that “friendly fire” from the immune system might be responsible for many severe COVID-19 cases. The explanation makes sense, considering that the main worry for doctors is the exacerbated immune response some patients develop. But the study pinpoints a type of malfunction inside the immune system that can actively worsen the COVID-19 prognosis. They say it’s autoantibodies that can attack healthy cells, including immune cells that would fight the SARS-CoV-2 virus, like B and T white blood cells. And the persistence of these autoantibodies might then induce Long COVID in patients, the illness where COVID-19 survivors keep experiencing symptoms weeks or even months after clearing the virus.
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The researchers published their findings on medRxiv, but the paper has not yet been reviewed by any peers. The Yale scientists used a technology called Rapid Extracellular Antigen Profiling (REAP) to screen 194 patients infected with the novel coronavirus against 2,770 extracellular and secreted proteins. They compared the COVID-19 cohort to a control group of 30 healthy hospital workers. Antibodies are proteins the immune system creates in response to pathogens like SARS-CoV-2. The current vaccines will teach the immune system to make antibodies that bind to the spike protein of the virus. That way, when the actual virus infects the body, the immune system will be able to block the virus from infecting lung cells immediately. Severe COVID-19 cases can be avoided this way. But there are also autoantibodies that are created and can target human cells erroneously. This is a known process in medicine that occurs in other illnesses, but with COVID-19, it can lead to complications. The researchers found that the autoantibodies would attack the body in various organs, including the brain, blood vessels, and the liver. The more autoantibodies circulating in a person's blood, the worse the illness would be. COVID-19 patients had “dramatic increases in autoantibody reactivities” compared to healthy individuals. More than 5% of the patients had autoantibodies to interferon, a key component of the immune system that’s first to respond to a pathogen like the novel coronavirus. A few days ago, a study identified five genes that favor severe COVID-19, including one that modulates interferon. That paper seemingly confirmed another interferon-related COVID-19 study from a few weeks ago that identified genetic issues with interferon genes as a risk factor for severe COVID-19. At the same time, a different paper said interferon autoantibodies might explain why some people experience severe cases. The Yale paper seems to confirm that research. Other autoantibodies also attacked B cells, which are involved in remembering past infections, and summoning neutralizing antibodies that can beat the virus. The autoantibodies also went for T cells. These are involved in killing infected cells and helping with the immune response throughout the infection. Other studies have shown that COVID-19 immunity hinges on neutralizing antibodies, B, and two T cell types. The white blood cells are present in large numbers even eight months after the illness, one of those studies said, suggesting that immunity might last longer than expected. The Yale researchers think that the combination of these different autoantibodies in the same patient might worsen the COVID-19 prognosis. Experiments on mice showed that the combination of autoantibodies would make them more susceptible to the infection, and more likely to die. “Covid-19 patients make autoantibodies that actually interfere with immune responses against the virus,” Yale immunobiologist Aaron Ring told The Guardian. “We certainly believe that these autoantibodies are harmful to patients with Covid-19.” The expert speculated that the effects could last after the virus is cleared. “Because antibodies can persist for a long time, it’s conceivable that they may contribute to the development of Long COVID diseases.” “Post-COVID syndromes could plausibly be caused by long-lived autoantibodies that persist well after the virus is cleared from the body,” Ring said. “If this is the case, there are immunosuppressive treatments, such as those used for rheumatological diseases, that could be effective.”
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It’s already proven that illnesses including rheumatoid arthritis, lupus, and multiple sclerosis occur because of problems with the immune response, including autoantibodies. The researchers found that COVID-19 patients had more autoantibodies than lupus patients. But research is still needed to prove the link between viral infection and autoimmune effects on the body. It’s not just COVID-19 that can leave long-lasting symptoms. Researchers are also investigating Ebola and Chikungunya for similar events. A Mayo Clinic doctor speculated a few days ago that Long COVID might last well over a year, basing his remarks on similar experiences with the SARS epidemic.
- Researchers from Yale might have discovered why some of the patients infected with the novel coronavirus develop severe forms of COVID-19.
- They found that patients with severe COVID-19 developed autoantibodies that attacked healthy cells instead of the virus, including interferon and B and T cells, thus hindering the immune response to the infection.
- The researchers speculate that this autoimmune response might favor Long COVID.
- If the hypothesis is correct, doctors will be able to formulate new therapies to treat patients experiencing long-term effects of the virus.
The more time passes, the more COVID-19 mysteries can be explained. Now, a team of Yale researchers might have just delivered what appears to be another breakthrough discovery. If their hypothesis is accurate, then the scientists might have provided the first explanation for Long COVID, the chronic type of coronavirus-like illness that follows the infection in some patients.
This team of researchers discovered that “friendly fire” from the immune system might be responsible for many severe COVID-19 cases. The explanation makes sense, considering that the main worry for doctors is the exacerbated immune response some patients develop. But the study pinpoints a type of malfunction inside the immune system that can actively worsen the COVID-19 prognosis. They say it’s autoantibodies that can attack healthy cells, including immune cells that would fight the SARS-CoV-2 virus, like B and T white blood cells. And the persistence of these autoantibodies might then induce Long COVID in patients, the illness where COVID-19 survivors keep experiencing symptoms weeks or even months after clearing the virus.
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Breakthrough discovery might reveal what causes Long COVID originally appeared on BGR.com on Mon, 14 Dec 2020 at 11:04:39 EDT. Please see our terms for use of feeds.