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COVID-19 & Autoimmune Disease: What We Know Now

August 25, 2020

While the world at large is still getting a handle on exactly how the coronavirus spreads, causes COVID-19, and affects people with autoimmune disease, what we know now is still a far cry from what we knew at the start.

As the number of studies on autoimmune disease and the coronavirus are climbing, we are beginning to see the similarities between the two and better understanding why certain conditions are high risk. There are instances in which having an autoimmune disease increases vulnerability to COVID-19 complications, and other cases where a coronavirus infection triggers autoimmune and other serious conditions.

What also holds true, is the distinctive way in which this virus impacts individuals – healthy or chronically ill, young or old. Like a fingerprint is unique to each person, your personal risk is unlike anyone else’s.

The High Risk List

The U.S. Center for Disease Control’s (CDC) latest list of high risk conditions defines a primary group including cancer, chronic kidney disease, COPD, immunocompromised from organ transplant, obesity, serious heart conditions, sickle cell disease, and type 2 diabetes, and a secondary group that may signal an increased risk for COVID-19 complications. This group includes but is not limited to asthma, cystic fibrosis, suppressed immune system, neurological conditions, liver disease, pulmonary fibrosis, smoking, and type 1 diabetes. For the full list, visit the CDC’s website.

While there is limited data on the specific conditions affected, it is worthwhile to note the autoimmune or autoimmune-related instances of the listed health issues. Autoimmune heart, lung, liver, and neurological diseases indicating a potentially increased risk may include:

Autoimmune myocarditis
Dressler’s syndrome
Subacute bacterial endocarditis
Cardiac sarcoidosis
Idiopathic pulmonary fibrosis
Autoimmune hepatitis
Multiple sclerosis
Guillain-Barre syndrome
Myasthenia gravis

Many systemic autoimmune diseases – lupus, rheumatoid arthritis, scleroderma, Sjogren’s – can cause serious problems in the heart, lungs, liver, and brain as well.

As stated on the CDC’s list, those on immunosuppressive medications like corticosteroids are also at higher risk for severe COVID-19 complications. However, keeping conditions in check and avoiding debilitating flare-ups may greatly outweigh the potential risks of a suppressed immune system.

 

COVID-19 Disproportionately Affects People of Color

Adding to the list of higher risk groups, COVID-19 disproportionately impacts communities of color (as do autoimmune diseases like lupus and scleroderma). Regarding COVID-19 cases in the United States from January through May, roughly 33% of persons were Hispanic, 22% were black, and 1.3% were American Indian/Alaska Native (1), despite the fact that these groups are part of the country’s minority population.

The racial disparities seen here are both a symptom and example of the systemic racism pervading American institutions. The high rates of underlying health conditions in communities of color, limited access to resources for COVID-19 testing and treatment, and economic hardships brought on by pandemic guidelines are all implicated in the added challenges faced by people of color (2, 3)

WHY ARE NON-RESPIRATORY DISEASES HIGH RISK?

As COVID-19 impacts the airways, COPD and other serious pulmonary diseases present a clear pathway to disaster. But how could seemingly unrelated conditions also turn a coronavirus infection into a life threatening event?

Organ systems depend on each other.

Heart disease (like autoimmune myocarditis), for instance, presents itself as an unlikely culprit in increased risk; however, normal operation of the heart is affected by other bodily functions. According to Dr. Maragakis, Senior Director of Infection Prevention at Johns Hopkins, the airways and lungs “work together with the heart to drive oxygen to the body’s tissues. When the lungs are overtaxed due to illness, the heart has to work harder” (4). This is a telling example of the vital connections between the different organ systems in our bodies.

The immune system’s response is the primary culprit.

We are learning that the source of the mayhem might not be the virus itself, but the immune system’s response to it. Severe COVID-19 cases may be associated with hyperactive immune responses in both chronically ill and healthy individuals. If you have an autoimmune disease, the immune system is already impaired – this may signal cause for concern.

“I HAVE AN AUTOIMMUNE DISEASE. AM I HIGH RISK?”

The answer is hazy. It remains unclear if having autoimmune disease automatically puts you at high risk for severe complications.

However, many sources point to no – unless you are also on immunosuppressive medication, are over 60 years old, or have one of the listed high risk conditions (like heart disease or obesity) in addition to autoimmune disease (5).

Many people with autoimmune disease and COVID-19 are asymptomatic or have mild to moderate symptoms and recover, some experience flare-ups or lingering effects, and others are hospitalized.

Apart from type 1 diabetes, most autoimmune diseases are not considered high risk because:

1. We do not have enough data

Studying autoimmune diseases in general is a daunting task, as there is still much unknown about these conditions and their etiology, or causes. To untangle a relationship between autoimmune disease and COVID-19 that may be relevant to the autoimmune community at large is a tall order.

2. From the data we do have, there are mixed outcomes

One review laid out the complicated forces at play in certain autoimmune diseases, demonstrating the need for further study and precaution. In systemic lupus erythematosus (SLE), the overexpression of a protein called ACE2 may be involved in severe COVID-19 cases. Researchers investigating the correlation between COVID-19 and rheumatic disease explain that ACE2 is a “functional receptor for the viral spike [of] glycoprotein, that allows the entry of SARS-CoV-2 into cells.” In some lupus patients, this phenomenon may correlate with increased susceptibility (6).

Other studies – the recent “SARS-CoV-2 infection among patients with systemic autoimmune diseases” conducted in Italy, a case series from New York reporting on “Covid-19 in Immune-Mediated Inflammatory Diseases”, and the “Epidemiology and Outcomes of Novel Coronavirus 2019 in Patients with Immune-Mediated Inflammatory Diseases” from the Global Rheumatology Alliance – found no higher risk of COVID-19 complications associated with autoimmune disease.

A review and meta-analysis on the association between severe or dead COVID-19 and autoimmune diseases showed that autoimmune disease was slightly associated with increased risk of severity and mortality of COVID-19” (7). They do clarify that the statistical difference was not significant, but that these findings do not stamp out the threat and more research is needed.

3. The impact of autoimmune disease and the behavior of the immune system are different in different people

While those living with autoimmune disease do experience altered immune system function, the ability to fight off pathogens is not necessarily weakened; rather the response is misguided.

Some people are more vulnerable to harmful bacteria and viruses, as their bodies are busy attacking their own tissues – or they are living with suppressed immune systems. For others, hyper-vigilant immune systems may prevent them from getting sick often. A body that overreacts to benign substances, like foods or harsh chemicals, may actually continue putting up a good fight when it comes to the real enemies: pathogenic microbes like the coronavirus (8, 9). It depends on the individual. 

It is possible for symptoms of COVID-19 to linger in people with chronic illnesses, despite a lack of severe symptoms and hospitalization. Both the CDC and a survey conducted by the Indiana University School of Medicine found that chronically ill patients who contracted the virus experienced a particularly long road to recovery, with lingering symptoms like fatigue and cough, as well as skin and neurological problems (10, 11).

Have you been feeling anxious and fatigued lately? Or experiencing more autoimmune flare-ups? Even if you’re not at high risk for serious COVID-19 complications, having a chronic illness means that stress is often a symptom trigger. And the pandemic is an endless symphony of worry, isolation, life changes, and other stressors. You’re not alone. After surveying arthritis patients, Creaky Joints reports that 42% of patients are experiencing an increase in fatigue during the pandemic.

AUTOIMMUNE SYMPTOM CONFUSION

It is not uncommon that some of your autoimmune symptoms mimic those of COVID-19. You may be wondering how to tell them apart. One telltale sign you might have coronavirus is the loss of taste and smell, which is not a common autoimmune symptom.

However, the data is still limited and there’s no hard-and-fast rule about which symptoms – like shortness of breath, fever, or fatigue – would signal presence of the virus and which would belong to an autoimmune flare-up.

Below are a few thoughts from rheumatologists – thanks to the Global Healthy Living Foundation and Creaky Joints:

  1. Rheumatic conditions (lupus, rheumatoid arthritis, scleroderma) do not seem to experience increased rates of infection or severe complications
  2. If you experience a coronavirus-like symptom (like fever), be aware of other symptoms that may indicate patterns consistent with a flare-up
  3. Notice if your dry cough, fever, fatigue, etc. is typical for your condition, or if it feels like something new

WHY ARE HEALTHY PEOPLE AFFECTED?

A preexisting, undetected – and possibly genetic – issue with the immune system may enable the virus to move from the nose and throat, and into the lungs (12, 13). Unable to produce the antibodies responsible for barring the virus entry into certain cells, which is how coronavirus multiplies, the body is thrown into submission and develops complications like pneumonia and acute respiratory distress syndrome (ARDS) (12).

Another reason some healthy people are ending up in the hospital has not been on our radar for long. Due to the COVID-19 pandemic, we are putting more of a spotlight on immune response. A seldom-used term – cytokine storm – is now circulating as fast as the viral infection itself.

Cytokine storm is a general descriptor for any number of “hyperactive immune response[s] characterized by the release of interferons, interleukins, tumor-necrosis factors, chemokines, and several other mediators”, explain researchers in their JAMA article, “Is a ‘Cytokine Storm’ Relevant to COVID-19?” Sky-high numbers of these molecules (generally lumped together under the umbrella term of cytokines) are released and can wreak havoc on the body.

The intensity of the response does not mean that the immune system is particularly good at fighting off invaders like the coronavirus. Rather, the off switch just doesn’t work. A bloated army of proinflammatory cytokines will remain on high alert and ready to fire well after the threat is over. Consequently, the immune system becomes chronically on-edge, which triggers actions against the body’s own cells. Herein lies the potentially deadly outcome, as it may eventually lead to multiple organ damage.

We also see the cytokine storm phenomena in some autoimmune diseases, like lupus and rheumatoid arthritis (14).

The use of the term “cytokine storm” to describe the pathophysiology of severe COVID-19 complications is still debated, however the theory has taken hold throughout the public and the scientific community, and brings a modicum of attention to immune-mediated events like autoimmunity.

Thankfully, severe complications in healthy individuals continue to be rare, and researchers are testing various drugs to dampen hyperactive immune responses. Typically used for autoimmune diseases like rheumatoid arthritis, biologics that affect specific cytokine receptors are currently being trialed as potential treatments (15).

CAN COVID-19 TRIGGER AUTOIMMUNE DISEASE?

The body’s immune response to the virus is the center of the story here, as well.

Other healthy individuals have experienced COVID-19 complications that result not in immediate lung disease or death, but in the triggering and potential development of autoimmune conditions.

In a University College of London Hospital’s study of 43 patients previously infected with the coronavirus, about 8 acquired Guillain-Barre syndrome and 9 acute disseminated encephalomyelitis (ADEM), both autoimmune diseases. The researchers suggest that this outcome was the result of the body’s immune response, rather than the virus itself.

Other studies have identified an overproduction of multiple autoantibodies in some COVID-19 patients. According to researchers investigating “The Correlation Between SARS-CoV-2 Infection and Rheumatic Disease”, such an event “is an important marker of autoimmune tolerance deficiency,” and may therefore signal a future of autoimmunity for those patients.

It is possible for COVID-19 to trigger the development of autoimmune disease or other post-infection fallout. After all, other pathogens – Epstein-Barr virus (EBV), Parvovirus B19, Rubella virus – have been implicated in the development of autoimmune diseases (13). Nevertheless, the numbers we have are small, and further research is needed to understand the true impact and substantiate this theory.

The Autoimmune COVID-19 Research Project

One way we’re understanding more about the effects of COVID-19 on autoimmune disease is through patient-centered initiatives like the Autoimmune COVID-19 Project, developed by the Global Healthy Living Foundation and Creaky Joints.

The authors of this longitudinal study are using online surveys to gather a broad spectrum of perspectives from individuals with autoimmune disease. Information requested includes symptoms, experiences with testing, telehealth, concerns about immunosuppressive therapy, and preferred sources of information about the virus.

Analyzing this data will produce a better understanding of the impact COVID-19 is having on quality of life. In this type of initiative, the experience of the patient is highly valued. Harnessing the expertise of researchers plus the power of patient voices will add a unique kind of knowledge to the conversation surrounding infectious disease today, as well as for future pandemics.

If you have been diagnosed with an autoimmune or related condition like rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, or vasculitis, you may participate in this study to help researchers gain more insight into the relationship between COVID-19 and autoimmune disease.

Our knowledge of autoimmune and the coronavirus is only going to increase, especially as the world gains a greater interest in the experiences and perspectives of the patients themselves.

REDUCING RISK

Just as nutrition and lifestyle factors can have profound impacts on our chronic conditions, so can they affect the way our bodies react when faced with COVID-19. The forms of prevention we’re almost too familiar with – hand washing, face masks, social distancing, testing, contact tracing – are not our only tools.

Nutrient-dense whole foods, restful sleep, daily movement, emotional support, and other necessities to human health impact how well the immune and other systems function. These seemingly benign factors are powerful enough to steer us towards either health or disease. If we’re able to make more healthful choices, then we can take some power back from the virus. 

Many people, however, are living without access to fresh foods, support, financial stability, comfortable housing, and resources to manage their autoimmune diseases, let alone incorporate diet and lifestyle changes. This is one reason why all the other methods we’re using to combat the coronavirus (yes, like face masks!) are equally important.

As always, risk should be assessed on a case-by-case basis. Outcomes depend on whether or not your disease is under control, you have multiple conditions, you’re taking medications, you experience racial inequities, you have access to quality care and resources, and a host of other factors with which we aren’t yet familiar.

Prevention Tips

Autoimmune Disease and Holistic Health Information

COVID-19 Resources from Organizations:

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Sources

  1. Article Footnotes
    1. Stokes, E., Zambrano, L., Anderson, K., Marder, E., Raz, K., Felix, S., Tie, Y., Fullerton, K. (June 19, 2020). Coronavirus Disease 2019 Case Surveillance — United States, January 22–May 30, 2020. Centers for Disease Control.

    2. Artiga, S., Garfield, R., Orgera, K. (April 7, 2020). Communities of Color at Higher Risk for Health and Economic Challenges due to COVID-19Kaiser Family Foundation.

    3. Wood, K. (May 6, 2020). A Diseased Nation: COVID-19 as a Deadly Symptom of Systemic Racism in the USMilken Institute.

    4. Maragakis, L. (June 25, 2020). Coronavirus and COVID-19: Who is at higher risk? Johns Hopkins Medicine.

    5. Gianfrancesco, M., Yazdany, J., Robinson, P. Epidemiology and outcomes of novel coronavirus 2019 in patients with immune-mediated inflammatory diseasesGlobal Rheumatology Alliance.

    6. Gao, Z., Wang, X., Lin, F., Dong, K. (May 1, 2020). The correlation between SARS-CoV-2 infection and rheumatic diseaseAutoimmunity Review, 2020 Jul; 19(7): 102557. doi: 10.1016/j.autrev.2020.102557

    7. Liu, M., Gao, Y. Zhang, Y., Shi, S., Chen, Y., Tian, J. (June 2, 2020). The association between severe or dead COVID-19 and autoimmune diseases: A systematic review and meta-analysisJournal of Infection, 2020 Sep; 81(3): e93-e95. doi: 10.1016/j.jinf.2020.05.065

    8. Callier, V. (July 29, 2016). Autoimmune diseases may be side effect of a strong immune systemNewScientist.

    9. Slazenger, S. (July 20, 2015). Inflammatory symptoms, immune system and food intolerance: One cause – many symptomsCell Science Systems.

    10. Kloss, K. (August 10, 2020). If You Have a Chronic Illness, You May Be at Higher Risk for Long-Lasting COVID-19 SymptomsCreaky Joints.

    11. Lambert, N. and Survivor Corps. (July 25, 2020). COVID-19 “Long Hauler” Symptoms Survey ReportIndiana University School of Medicine.

    12. Cyranoski, D. (May 4, 2020). Profile of a killer: the complex biology powering the coronavirus pandemicNature.

    13. Ehrenfeld, M., Tincani, A., Andreoli, L., Cattalini, M., Greenbaum, A., Kanduc, D., Alijotas-Reig, J., Zinserling, V., Semenova, N., Amital, H., Shoenfeld, Y. (June 11, 2020). Covid-19 and autoimmunityAutoimmunity Review, 2020 Aug; 19(8): 102597. doi: 10.1016/j.autrev.2020.102597

    14. Windsor, M. (November 1, 2019). Here’s a playbook for stopping deadly cytokine storm syndromeUniversity of Alabama at Birmingham: Reporter.

    15. Williams, D. (April 21, 2020). Could Curbing Runaway Immune Responses Treat COVID-19? The Scientist.

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