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The Long-Term Effects of COVID-19: Is Autoimmunity to Blame?

Emma

Updated on - Written by
Medically reviewed by Kathy Shattler, MS, RDN

The long-term effects of COVID[1] and its underlying causes have eluded healthcare professionals in the scientific community since the onset of the pandemic. “Long COVID,”[2] as it’s been called, describes coronavirus victims whose symptoms last much longer than your usual cold or flu.

Researchers are taking a new interest in one interesting aspect of how the body reacts to a COVID-19 infection. This reaction may be able to explain why COVID-like symptoms can sometimes persist even months after being neutralized. Is autoimmunity the culprit behind COVID in the long term?

What Is “Long-COVID”?

Long COVID is a catch-all term that refers to an extended bout of COVID and any of the associated symptoms therein.

Some of the symptoms[3] characteristic of a long-term COVID infection include:

  • Shortness of breath and respiratory distress
  • Fatigue and a lack of energy
  • Difficulty exerting oneself without becoming exhausted
  • Brain fog, or an unusual lack of focus
  • Coughing and sneezing
  • Chest pain
  • Abdominal pain
  • Light-headedness and dizziness
  • Changes in the ability to taste and smell
  • Other forms of bodily dysfunction, such as fever, diarrhea, insomnia, and headaches

Post-COVID conditions are generally defined as pervasive symptomatology four or more weeks after contracting the coronavirus. Its exact cause is still currently disputed amongst the greater scientific community, but brand new evidence on how the body reckons with COVID-19 long after first contact may have us on the right track.

What Does This New Research Show?

This landmark study [4] in the New England Journal of Medicine published just last month explores one intriguing new possibility underlying COVID’s ability to remain active within its host for extended, indefinite periods of time.

It lays out a process of recognition that the cells of the body carry out when they meet something foreign to your DNA. This process is how it decides whether or not to attack something as an intruder. Any unknown agent in the body is referred to as an antigen — bacteria, random dust particles, and other impurities all fit the bill.

The immune system does its best to eradicate whatever it finds using defensive cells called antibodies, and, oftentimes, that’ll be the end of it. Other times, however, these antibodies get just a little bit too involved with the invading particle or organism.

An antibody’s outer surface is adorned with immunogenic regions, used to bind with antigens to neutralize them. Many complex chemical reactions ensue, and new compounds come into being as a byproduct of these interactions.

According to this new research, there might be something about this new chemical byproduct that attracts different, separate classes of antibodies responsible for other defensive work to the site of the interaction, like sharks to blood in the water[5]. They then attack the original, post-antigen antibodies, either confused as to their true identities or destroying them specifically to attack the neutralized antigens that they bear.

These “zombie cells” may, in some cases, resemble the original antigen in shape so closely that they then simply continue to carry out the antigen’s original intention. This mimicking effect is so minute that the post-antigen antibodies are able to bind to the same targeted cell receptors that the antigens were aiming for in the first place.

This phenomenon is classified as an autoimmune function. What exactly does this term mean?

What Is Autoimmunity? What Does It Have to Do With Long-COVID?

An autoimmune disorder[6] is an immune response that attacks a cell that’s part of your body. Some common examples of autoimmune disease include:

Because the autoimmune response to the antigen-laden antibodies strikes them down in the midst of their struggle against the virus, the oncoming second wave of antibodies might be disrupting the neutralization process.

This constant stopping and starting leave the victim in a perpetual state of half-sickness. On top of this, the antigens’ ability to hijack antibodies prevents them from being fully neutralized, as they’re still able to continue binding to new, healthy cells from the surface of the antibody.

Ongoing research into this aspect of the coronavirus has revealed a lot about how the battle is won on a cellular level and the forces that determine victory or defeat for your natural lines of defense. While this is far from the end of the line, what we know so far is promising.

For now, it’s got a lot of people talking. The notion might be able to help us unlock the secret to a more effective treatment for COVID and even predict how susceptible a given person might be to contracting it. Perhaps the answer isn’t necessarily to destroy the COVID antigens themselves — instead, preventing this autoimmune interruption from occurring might be a more effective solution.

It’s a fascinating train of thought. Things aren’t always as they seem, and this new insight turns the problem completely on its head.

Is Autoimmunity the Key?

Curing COVID in the short term has proven to be difficult enough. When you take the long-term implications of its tenacity into consideration, however, things only become exponentially more complex. Autoimmunity adds another layer to the puzzle; our bodies incubate the virus long-term, protecting it from us indefinitely.

With every new breakthrough that the scientific community makes, we cover new ground on the road to our final victory over the COVID-19 disaster. Only time will tell where this path will lead us, but the outlook currently is more than optimistic.


+ 9 sources

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  1. López-León, S., Wegman-Ostrosky, T., Perelman, C., Sepulveda, R., Rebolledo, P.A., Cuapio, A. and Villapol, S. (2021). More than 50 Long-Term Effects of COVID-19: A Systematic Review and Meta-Analysis. SSRN Electronic Journal. [online] Available at: https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3769978 [Accessed 24 Dec. 2021].
  2. Mahase, E. (2020). Covid-19: What do we know about “long covid”?. BMJ, [online] p.m2815. Available at: https://www.bmj.com/content/370/bmj.m2815.long [Accessed 24 Dec. 2021].
  3. CDC (2020). Post-COVID Conditions. [online] Centers for Disease Control and Prevention. Available at: https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html [Accessed 24 Dec. 2021].
  4. Murphy, W.J. and Longo, D.L. (2021). A Possible Role for Anti-idiotype Antibodies in SARS-CoV-2 Infection and Vaccination. New England Journal of Medicine. [online] Available at: https://www.nejm.org/doi/full/10.1056/NEJMcibr2113694 [Accessed 24 Dec. 2021].
  5. Pan, Y., Yuhasz, S.C. and Amzel, L.M. (1995). Anti‐idiotypic antibodies: biological function and structural studies. The FASEB Journal, [online] 9(1), pp.43–49. Available at: https://pubmed.ncbi.nlm.nih.gov/7821758/ [Accessed 24 Dec. 2021].
  6. Rosenblum, M.D., Remedios, K.A. and Abbas, A.K. (2015). Mechanisms of human autoimmunity. Journal of Clinical Investigation, [online] 125(6), pp.2228–2233. Available at: https://www.jci.org/articles/view/78088 [Accessed 24 Dec. 2021].
  7. Anon, (2021). Rheumatoid Arthritis (RA). [online] Available at: https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html [Accessed 24 Dec. 2021].
  8. Anon, (2021). Psoriasis. [online] Available at: https://www.cdc.gov/psoriasis/index.htm [Accessed 24 Dec. 2021].
  9. Nih.gov. (2021). Multiple Sclerosis Information Page | National Institute of Neurological Disorders and Stroke. [online] Available at: https://www.ninds.nih.gov/Disorders/All-Disorders/Multiple-Sclerosis-Information-Page [Accessed 24 Dec. 2021].

Emma

Medically reviewed by:

Kathy Shattler

Emma Garofalo is a writer based in Pittsburgh, PA. A lover of science, art, and all things culinary, few things excite her more than the opportunity to learn about something new." It is now in the sheet in the onboarding paperwork, apologies!!

Medically reviewed by:

Kathy Shattler

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