‘Long COVID’ may not be connected to severity after all

As the pandemic drags on, the number of people with long-haul symptoms post-infection seems to be on the rise.

“Long COVID” brings with it a host of debilitating symptoms, including extreme fatigue, shortness of breath, brain fog or memory problems, difficulty falling or staying asleep, heart palpitations, tinnitus or ringing in the ears and joint and muscle pain. It’s also been linked with persistent thyroid inflammation.

So far, it’s been somewhat of a mystery why some people who’ve had COVID-19 suffer from “long COVID” and others escape the phenomenon. Some research has linked long-haul symptoms with micro clots, tiny clots inside the clots caused by COVID-19 that are packed with inflammatory molecules. And another study found that people previously infected with Epstein Barr, the virus that causes mono, could be at higher risk of long COVID.

There’s also been at least one study suggesting that long COVID mainly affects those who have had more than 5 of the 10 most common COVID-19 symptoms. This would suggest people with long COVID had a more severe case of the illness.

But a recent study from Cedars-Sinai may have debunked the notion that only severe cases of COVID-19 lead to its long-haul form…

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Autoantibodies present even in mild COVID-19 cases

The study found infection with SARS-CoV-2, the virus that causes COVID-19, can trigger an overactive immune response that lasts well after the infected person recovers—even if they had mild or no symptoms.

The issue lies in self-attacking proteins called autoantibodies. Usually, when a virus or other pathogen infects a person, their body releases antibodies that detect these foreign interlopers and keep them from invading cells.

But in cases when the immune system is overstressed, the infected person produces autoantibodies, which attack their own organs and tissues and can persist over time. These autoantibodies are often present in people who have autoimmune diseases in which the body attacks itself, such as lupus and rheumatoid arthritis.

Researchers found that all the people in the study who had confirmed evidence of a previous SARS-CoV-2 infection had elevated levels of a wide variety of autoantibodies present up to six months after full recovery from COVID-19.

While previous research has confirmed the presence of autoantibodies in people with severe cases of COVID-19, this is the first study to report both the presence of autoantibodies in people with mild or asymptomatic infection and their persistence over time.

“These findings help to explain what makes COVID-19 an especially unique disease,” says Dr. Justyna Fert-Bober, research scientist at Cedars-Sinai’s Smidt Heart Institute and co-senior author of the study. “These patterns of immune dysregulation could be underlying the different types of persistent symptoms we see in people who go on to develop the condition now referred to as long COVID-19.”

“We found signals of autoantibody activity that are usually linked to chronic inflammation and injury involving specific organ systems and tissues such as the joints, skin and nervous system,” says Dr. Susan Cheng, director of the Institute for Research on Healthy Aging at the Smidt Heart Institute and co-senior author of the study.

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Men more likely to have post-COVID autoantibodies

One interesting finding is that men had a higher number of elevated autoantibodies than women. This runs counter to previous research that found women — particularly those under the age of 50 — were more likely to experience long COVID than men.

“On the one hand, this finding is paradoxical given that autoimmune conditions are usually more common in females,” Dr. Fert-Bober says. “On the other hand, it is also somewhat expected given all that we know about males being more vulnerable to the most severe forms of COVID-19.”

The researchers intend to expand the study to look for the specific types of autoantibodies that might be present and persist in people with long-haul COVID-19 symptoms. Also, since the current study was in people infected before vaccines became widely available, researchers will take a close look at whether people with breakthrough infections generate similar autoantibodies.

“If we can better understand these autoantibody responses, and how it is that SARS-CoV-2 infection triggers and drives these variable responses, then we can get one step closer to identifying ways to treat and even prevent these effects from developing in people at risk,” Dr. Cheng says.

During the pandemic, vitamin D really took the spotlight. And there’s a link that’s important to mention, though it was not part of this particular study…

Low vitamin D has been found to raise the risk for respiratory infections and additionally, some studies performed over the last two pandemic years have linked low vitamin D levels with higher rates of infection and mortality.

Oddly enough, past research has also found a connection between low levels of the vitamin and autoimmune diseases.

Sources:

COVID-19 Can Trigger Self-Attacking Antibodies — Cedars-Sinai

Paradoxical sex-specific patterns of autoantibody response to SARS-CoV-2 infection — Journal of Translational Medicine