COVID-19 can disrupt the immune system in ways that may increase the risk of developing autoimmune diseases or triggering flare-ups of existing autoimmune conditions in some people. Researchers believe mechanisms such as molecular mimicry, persistent immune activation and loss of immune tolerance may contribute, but COVID does not cause autoimmune disease in everyone. Most people recover without developing autoimmunity, and scientists are still working to understand who is most at risk.
Key Takeaways
- COVID-19 can alter immune function, potentially increasing the risk of autoimmune diseases in a small subset of people.
- Autoimmune diseases occur when the immune system mistakenly attacks healthy tissues instead of protecting them.
- Researchers are investigating mechanisms including molecular mimicry, persistent immune activation and immune dysregulation.
- Long COVID and autoimmune diseases share many symptoms, but they are not the same condition.
- Current evidence suggests genetics, existing autoimmune conditions and individual immune responses influence who develops post-COVID autoimmunity.
Introduction
COVID autoimmune disease is a topic receiving increasing attention as researchers investigate whether COVID-19 can trigger new autoimmune diseases or worsen existing ones. Although most people recover completely, scientists are exploring how SARS-CoV-2 may disrupt immune regulation in a small number of susceptible individuals.
If you’ve developed new symptoms after COVID-19, you may have wondered whether the virus has somehow changed your immune system.
For some people, the answer may be yes.
Over the past few years, researchers have found that COVID-19 can leave lasting effects on the immune system long after the initial infection has resolved. While most people recover without long-term complications, others develop persistent immune abnormalities that may contribute to Long COVID, trigger flare-ups of existing autoimmune diseases or, in some cases, precede the development of new autoimmune conditions.
This doesn’t mean COVID-19 automatically causes autoimmune disease. Rather, it appears to act as a trigger in people who are already biologically susceptible. Understanding how this happens is becoming one of the most important areas of Long COVID research.
What Is an Autoimmune Disease?
Your immune system is designed to recognise harmful viruses, bacteria and other threats while leaving your own tissues alone.
In autoimmune diseases, this process breaks down.
Instead of distinguishing between “self” and “foreign”, the immune system mistakenly attacks healthy cells, causing inflammation and tissue damage. Depending on which tissues are affected, this can lead to conditions such as rheumatoid arthritis, Sjögren’s syndrome, Hashimoto’s thyroiditis, lupus or multiple sclerosis.
Many autoimmune diseases develop gradually over months or even years. Genetics often play an important role, but environmental triggers—including viral infections—can also contribute.
COVID-19 is now one of several infections being investigated for its potential role in triggering autoimmune responses.
Can COVID Trigger Autoimmune Diseases?
The short answer is yes but only in some people.
Large population studies have found that people recovering from COVID-19 appear to have a slightly higher risk of developing certain autoimmune diseases compared with people who have not had the infection. Researchers have reported increased diagnoses of conditions affecting the thyroid, joints, nervous system and connective tissues following COVID-19.
However, it’s important to keep these findings in perspective.
Most people who develop COVID-19 do not go on to develop an autoimmune disease. The increased risk appears to affect only a relatively small proportion of people and is thought to depend on factors such as genetics, age, sex, the severity of the initial infection and pre-existing immune abnormalities.
Rather than creating autoimmune disease from nothing, COVID-19 may act as the event that tips an already vulnerable immune system into a state of chronic dysregulation.
How Could COVID Trigger Autoimmunity?
Scientists believe several biological mechanisms may contribute. These mechanisms are not mutually exclusive and may occur together in different people.
Molecular Mimicry
Some proteins produced by SARS-CoV-2 resemble proteins naturally found in the human body.
This similarity may confuse the immune system, causing antibodies or immune cells generated to fight the virus to mistakenly recognise healthy tissues as foreign. This process, known as molecular mimicry, has been proposed as one explanation for post-infectious autoimmune diseases.
Persistent Immune Activation
Even after the virus has been cleared, some people continue to show signs of immune activation.
Inflammatory signals remain elevated, immune cells fail to fully return to their resting state and the immune system may continue responding as though a threat is still present. Over time, this prolonged activation could increase the likelihood of autoimmune reactions.
Loss of Immune Tolerance
A healthy immune system has built-in mechanisms that prevent it from attacking the body’s own tissues.
COVID-19 may temporarily disrupt these regulatory processes in susceptible individuals, reducing the immune system’s ability to distinguish between harmful pathogens and healthy cells.
Viral Persistence
Another leading theory is that fragments of SARS-CoV-2 may remain in certain tissues after the initial infection.
Rather than causing active infection, these viral remnants may continue stimulating the immune system, contributing to ongoing inflammation and immune dysregulation in some people. This remains an active area of research and is unlikely to explain every case of Long COVID.
Which Autoimmune Diseases Have Been Linked to COVID-19?
Researchers have reported an increased risk of several autoimmune diseases following COVID-19. However, the strength of the evidence varies considerably between conditions.
Some diseases, such as Guillain-Barré syndrome and autoimmune thyroid disease, have relatively well-established associations with viral infections. Others are supported mainly by observational studies, case reports or ongoing research.
Importantly, an association does not prove that COVID-19 directly caused the disease. In many cases, the infection may simply act as a trigger in someone who was already genetically predisposed to developing autoimmunity.
| Autoimmune disease | Current evidence after COVID-19 | What researchers have observed |
|---|---|---|
| Hashimoto’s thyroiditis | Moderate | New diagnoses and worsening thyroid dysfunction have been reported after COVID-19. |
| Sjögren’s syndrome | Emerging | COVID may trigger symptoms or unmask previously undiagnosed disease in susceptible people. |
| Rheumatoid arthritis | Moderate | Both new-onset disease and flare-ups have been described following infection. |
| Systemic lupus erythematosus (SLE) | Emerging | Case reports and observational studies suggest COVID may trigger disease activity. |
| Multiple sclerosis (MS) | Limited | Relapses have been reported, although evidence for new disease remains limited. |
| Guillain-Barré syndrome (GBS) | Strong but rare | A recognised autoimmune neurological complication that can occur after viral infections, including COVID-19. |
| Myasthenia gravis | Limited | New cases and symptom worsening have been reported but remain uncommon. |
| Coeliac disease | Limited | Research is ongoing and evidence is currently weak. |
Does Long COVID Mean You Have an Autoimmune Disease?
No.
Although Long COVID and autoimmune diseases share many symptoms, they are not the same condition.
Both can cause:
- profound fatigue
- joint and muscle pain
- brain fog
- dry eyes and dry mouth
- autonomic symptoms
- headaches
- exercise intolerance
However, having these symptoms does not automatically mean you have an autoimmune disease.
Many people with Long COVID have completely normal autoimmune blood tests, while others have immune abnormalities that do not meet the criteria for a specific autoimmune diagnosis.
Researchers increasingly believe Long COVID is a heterogeneous condition, meaning different biological mechanisms may dominate in different people. For some, viral persistence may be the main driver. Others may have immune dysregulation, vascular dysfunction, autonomic impairment or metabolic abnormalities.
Autoimmunity is therefore considered one possible pathway, rather than a universal explanation for Long COVID.
Who Is Most at Risk?
Researchers are still trying to understand why COVID-19 appears to trigger autoimmune diseases in some people but not others.
Current evidence suggests the risk may be higher in people who:
- have a family history of autoimmune disease
- already have an autoimmune condition
- are female, as most autoimmune diseases are more common in women
- experienced severe COVID-19 or significant immune activation
- have certain genetic factors that influence immune regulation
These factors increase susceptibility but do not guarantee that someone will develop an autoimmune disease after COVID-19.
When Should You Speak to Your GP?
Persistent fatigue alone does not usually indicate an autoimmune disease.
However, you should seek medical assessment if, after COVID-19, you develop symptoms such as:
- persistent joint swelling or prolonged morning stiffness
- unexplained skin rashes
- dry eyes or dry mouth that continue for several months
- muscle weakness rather than fatigue
- numbness or tingling
- unexplained weight changes
- recurrent mouth ulcers
- swollen glands
- symptoms that continue to worsen rather than gradually improve
Depending on your symptoms, your GP may recommend blood tests for inflammatory markers, thyroid function, autoimmune antibodies or refer you to a rheumatologist, neurologist or another specialist.
Conclusion
COVID-19 has transformed our understanding of how viral infections can affect the immune system. Although most people recover without developing autoimmune disease, growing evidence suggests the virus may trigger or accelerate autoimmune processes in a small number of susceptible individuals.
At the same time, Long COVID is not simply an autoimmune disease. It is increasingly recognised as a complex condition involving overlapping mechanisms, including immune dysregulation, viral persistence, vascular dysfunction and autonomic nervous system changes.
Understanding which biological pathway is driving symptoms in each individual is likely to be one of the biggest challenges and opportunities for future Long COVID research and treatment.
requently Asked Questions
Can COVID trigger an autoimmune disease?
Yes, it can—but it appears to happen in only a small proportion of people. Current research suggests COVID-19 may trigger or unmask autoimmune diseases in individuals who are already genetically or biologically susceptible. Most people recover without developing an autoimmune condition, and researchers are still investigating why some people are affected while others are not.
How do I know if my symptoms are Long COVID or an autoimmune disease?
Many symptoms overlap, including fatigue, joint pain, brain fog, muscle aches and dry eyes or mouth. However, Long COVID does not automatically mean you have an autoimmune disease. If symptoms persist, worsen or are accompanied by signs such as joint swelling, persistent rashes or muscle weakness, your healthcare provider may recommend further investigations, including autoimmune blood tests.
Can COVID make an existing autoimmune disease worse?
Yes. Many people with conditions such as rheumatoid arthritis, lupus, Sjögren’s syndrome or multiple sclerosis have reported flare-ups following COVID-19. The infection can temporarily increase immune activity, which may worsen symptoms or trigger a disease flare in some individuals. Ongoing management should always be discussed with your specialist.
Can autoimmune diseases caused by COVID be treated?
There is currently no specific treatment for autoimmune diseases triggered by COVID-19. Treatment depends on the condition diagnosed and the symptoms experienced. Many autoimmune diseases can be managed with medications that reduce inflammation or regulate the immune system, alongside supportive care. Early diagnosis is important, as prompt treatment may help prevent complications and improve quality of life.
edical Disclaimer
This article is for educational purposes only and should not be considered medical advice. Research into Long COVID and autoimmune diseases is evolving rapidly, and scientists are still investigating how COVID-19 may contribute to immune dysregulation and the development of autoimmune conditions.
Not everyone who develops Long COVID has an autoimmune disease, and not everyone who develops an autoimmune disease has previously had COVID-19. If you have persistent symptoms, new neurological problems, joint swelling, unexplained rashes, or other concerning signs, seek advice from a qualified healthcare professional.
Never start, stop or change prescribed medications without discussing them with your healthcare provider.
Key References
Davis HE, McCorkell L, Vogel JM, Topol EJ.
Long COVID: major findings, mechanisms and recommendations.
Nature Reviews Microbiology. 2023.
Wang W, Wang CY, Wang SI, et al.
COVID-19 and the risk of autoimmune diseases: a population-based cohort study.
eClinicalMedicine (The Lancet Discovery Science). 2023.
Chang SE, Feng A, Meng W, et al.
New-onset IgG autoantibodies in hospitalized patients with COVID-19.
Nature Communications. 2021.
NIH RECOVER Initiative
https://recovercovid.org
National Institute for Health and Care Research (NIHR) – Long COVID Research
https://www.nihr.ac.uk
Nature Reviews Rheumatology – Reviews on COVID-19 and autoimmune disease.
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