Infection vs vaccination: which really raises autoimmune disease risk?
Some like to blame vaccines for dangerous autoimmune issues, but the evidence is clear: the infections they help prevent are the bigger risk.
- 30 March 2026
- 6 min read
- by Linda Geddes
At a glance
- A range of viral, bacterial, fungal and parasitic infections have been linked to the development of autoimmune conditions.
- Vaccines can, in very rare cases, be linked to autoimmune responses, but this is far less common than after infection. For example, both influenza and influenza vaccination have been associated with Guillain-Barré syndrome, but the risk is much higher after infection. One study in Ontario found around one case per million vaccinations, compared with 17 per million influenza infections.
- Vaccination is often the best way to reduce the risk of infection-related complications, including autoimmunity, by giving the immune system a controlled glimpse of a pathogen, without the prolonged infection and inflammation that can push it off course.
Claims that vaccines can trigger autoimmune disease have circulated for years. But the far bigger and better-established risk comes from infection itself.
When the immune system turns against the body, the consequences can be serious. This process underpins conditions ranging from multiple sclerosis to lupus and can cause symptoms from fatigue and joint pain to long-term organ damage.
Vaccines give the immune system a controlled glimpse of a pathogen, without the prolonged infection and inflammation that are more likely to push it off course.
At its core, autoimmunity happens when the immune system loses its ability to distinguish between harmful invaders and the body’s own tissues, sometimes producing autoantibodies: misguided proteins that attack healthy cells instead of bacteria or viruses.
Yet, while immune responses to infection are common, this kind of misfiring is not: autoimmunity is rare and cases linked to vaccination are rarer still.
Which infections have been linked to autoimmunity?
A wide range of viral, bacterial, fungal and parasitic infections have been linked to the development of autoimmune responses.
Some of the strongest evidence relates to Group A Streptococcus, a bacterium that often lives harmlessly on the skin or in the throat but can sometimes cause illnesses ranging from ‘strep throat’ and scarlet fever to skin and soft tissue infections, and life-threatening toxic shock syndrome.
These infections have also been linked to several autoimmune diseases, including acute rheumatic fever, characterised by joint and heart inflammation and sometimes chronic heart problems; vasculitis, in which blood vessels become inflamed, reducing blood flow to organs and tissues; and PANDAS, a condition that can trigger the sudden onset of obsessive-compulsive behaviours or tic disorders in children.
Campylobacter jejuni is another bacterium that can trigger autoimmune disease, most notably Guillain-Barré syndrome, a condition in which the immune system attacks the peripheral nerves, leading to muscle weakness and, in severe cases, paralysis.
Then there’s Epstein-Barr virus, best known for causing glandular fever, but which has also been linked to several autoimmune diseases, including multiple sclerosis, lupus and Sjögren’s syndrome.
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Beyond these examples, there is mounting evidence that immune dysregulation, including possible autoimmune responses, may play a role in a range of long-term post-infectious syndromes, including Long COVID, Lyme disease and conditions following infections such as chikungunya and Ebola.
“When you look for autoantibodies after infection, you find them, and you find them in a way that looks plausible as a possible driver of that disease process,” said Prof Danny Altmann at Imperial College London, who is studying the mechanisms linking infection and autoimmunity.
How do infections trigger autoimmunity?
A lot remains unknown, including why some people develop autoimmunity while the vast majority recover relatively unscathed.
For instance, more than 95% of people are infected with Epstein-Barr virus, yet only a tiny fraction – under 1% – will develop conditions such as multiple sclerosis or, more rarely, lupus.
“On the other hand, if you haven’t got Epstein-Barr virus, you’ve got almost no chance of having those diseases,” said Altmann.
Genetic factors are almost certainly involved, along with age, sex and environmental influences, such as which infections a person has been exposed to, when they occur and how the immune system responds.
When it does happen, autoimmunity appears to arise when the immune system mistakenly recognises the body’s own tissues as foreign, or these tissues are caught in the crossfire of an immune response to infection.
One potential mechanism under investigation is known as molecular mimicry. This occurs when a virus or bacterium carries proteins that closely resemble those found in the human body.
As the immune system learns to attack the pathogen, it may also target tissues carrying similar proteins. Epstein-Barr virus, for instance, produces proteins that resemble components of myelin – the protective coating that wraps around nerve fibres – potentially contributing to the development of multiple sclerosis.
Another potential mechanism is so-called bystander activation. This occurs when an infection causes widespread inflammation that activates immune cells more broadly than intended. In the process, some immune cells that can react to the body’s own tissues may be switched on as collateral damage.
In most cases, this response is short-lived, but in some people it may contribute to longer-term autoimmune disease.
Then there’s epitope spreading, in which an immune response initially directed at a virus or bacterium gradually broadens to target the body’s tissues.
As infection causes tissue damage, proteins that the immune system does not usually encounter may be released and taken up by immune cells, which then begin to recognise and attack them as well.
In reality, scientific understanding of these mechanisms is “a work in process”. It is possible that different mechanisms are in play in different infections and there are many other avenues to explore, Altmann said.
Can vaccines trigger autoimmune disease?
Vaccines can trigger autoimmune responses but it is extremely rare, and far less common than autoimmunity triggered by infection, which is itself very rare. In fact, vaccination is often the best way to reduce that risk.
Vaccines give the immune system a controlled glimpse of a pathogen, without the prolonged infection and inflammation that are more likely to push it off course.
For instance, the risk of myocarditis (inflamed heart muscle) after COVID-19 infection has been estimated at around 146 cases per 100,000 infections. After mRNA vaccination it’s much lower – about two cases per 100,000 people. Other studies suggest between 0.3 and 5 cases per 100,000, with most cases mild and resolving quickly.
Guillain-Barré syndrome is another autoimmune disorder linked to infections. Most people recover, but some are left with long-term nerve damage, and in rare cases it can be fatal. About one in every 1,000 people infected with Campylobacter develops Guillain-Barré syndrome.
Influenza has also been linked to Guillain-Barré syndrome, as has influenza vaccination. But again, the risk is much higher after infection. One study in Ontario, Canada, found around 1 case per million vaccinations, compared with 17 per million influenza infections.
Taken together, these findings suggest that while vaccines can very rarely be associated with autoimmune conditions, infection itself presents a far higher risk.
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