Guillain-Barré syndrome (GBS) is caused by the immune system mistakenly attacking the body’s own peripheral nerves, typically triggered by a preceding infection. About two thirds of people diagnosed with GBS report symptoms of a respiratory or gastrointestinal infection in the six weeks before their symptoms begin. The exact reason some people develop GBS after a common infection while most don’t remains unknown.
How the Immune System Turns on Itself
The core problem in GBS is a case of mistaken identity. When you fight off an infection, your immune system produces antibodies tailored to recognize and destroy the invading bacteria or virus. In GBS, certain molecules on the surface of the infectious organism look structurally similar to molecules on your peripheral nerves. This resemblance, called molecular mimicry, causes the antibodies to attack healthy nerve tissue after the infection clears.
The attack can target two different parts of the nerve. In the most common form, called AIDP, the immune system strips away the protective insulation (myelin sheath) that surrounds nerve fibers. Without this insulation, electrical signals slow down or stop entirely, causing weakness and numbness. In another form called AMAN, the immune system goes after the nerve fiber itself rather than the insulation. AMAN tends to cause purely motor symptoms, meaning muscle weakness without the tingling or numbness. A related variant, AMSAN, damages both the nerve fiber and its insulation, affecting both sensation and movement.
Campylobacter: The Most Common Bacterial Trigger
The single most well-established trigger for GBS is infection with Campylobacter jejuni, a bacterium that causes food poisoning. At least 1 in 20 people with GBS had a recent Campylobacter infection, and some studies put that number as high as 8 in 20. The connection is so well documented that it serves as the textbook example of molecular mimicry in autoimmune disease: sugar molecules on the surface of Campylobacter are nearly identical to sugar molecules found on nerve cell membranes.
To be clear, the vast majority of people who get Campylobacter food poisoning never develop GBS. The infection is extremely common, while GBS remains rare. Something about an individual’s immune response, likely influenced by genetics, determines whether the crossover attack on nerve tissue happens.
Viruses That Can Trigger GBS
Several viral infections are confirmed triggers. These include cytomegalovirus (a common virus that most people carry without symptoms), Epstein-Barr virus (the cause of mono), influenza, and Zika virus. The Zika outbreak in 2015 and 2016 drew particular attention after GBS cases surged in affected regions.
COVID-19 has joined that list. An Israeli study found the odds of developing GBS were about six times higher after a COVID-19 infection compared to people without a recent infection. Among 76 GBS patients studied, nearly 12% had tested positive for COVID-19 in the preceding weeks, compared to just 2.4% in the control group. This puts COVID-19 alongside other respiratory infections as a meaningful trigger, though the absolute risk for any individual remains very low.
Vaccines and GBS Risk
The link between vaccines and GBS is real but extremely small. The most notable case occurred in 1976, when a swine flu vaccine was associated with roughly one additional GBS case per 100,000 people vaccinated. For modern seasonal flu vaccines, when any increased risk has been detected, it has consistently fallen in the range of 1 to 2 additional cases per million doses.
For COVID-19 vaccines specifically, CDC studies found evidence of an increased GBS risk after the Johnson & Johnson/Janssen vaccine (which used a viral vector technology) but not after the Pfizer or Moderna mRNA vaccines. In fact, the Israeli study found that mRNA vaccination was associated with a decreased risk of GBS, possibly because it reduced the chance of a COVID-19 infection, which itself is a stronger trigger.
Each year in the United States, between 3,000 and 6,000 people develop GBS regardless of vaccination. The background rate matters here: GBS happens with or without vaccines, and infections remain the dominant trigger.
Surgery, Trauma, and Other Rare Triggers
Infections account for most cases, but GBS can occasionally follow surgery or physical trauma. Hodgkin lymphoma has also been identified as a trigger. In all of these situations, the suspected mechanism is the same: something activates or disrupts the immune system in a way that leads to the crossover attack on peripheral nerves. These non-infectious triggers are considerably rarer and less well understood than the infectious ones.
Who Is Most at Risk
GBS affects roughly 1.1 people per 100,000 worldwide each year. Men are about 40% more likely to develop it than women, with an incidence of 1.38 per 100,000 compared to 0.99 per 100,000 for women. The reasons for this gender difference aren’t fully understood.
Risk also increases with age. Children and teenagers have the lowest incidence at about 0.48 per 100,000, while adults over 70 face the highest rate at 1.59 per 100,000. This age pattern may reflect cumulative changes in immune regulation, a greater likelihood of triggering infections, or both. Still, GBS can strike at any age, including in otherwise healthy young adults.
Why Only Some People Develop GBS
This is the central unanswered question. Campylobacter infections alone cause an estimated 1.5 million illnesses per year in the U.S., yet only a tiny fraction of those people go on to develop GBS. The same is true for every other known trigger. The infection or event appears to be necessary but not sufficient on its own.
The leading explanation is that individual variation in the immune system, shaped by genetics and possibly by the specific strain of the infecting organism, determines who crosses the line from a normal immune response to one that damages nerves. Certain strains of Campylobacter, for instance, carry surface molecules that more closely mimic nerve tissue than others, making the crossover attack more likely. But even exposure to those high-risk strains rarely causes GBS, suggesting that the host’s immune makeup plays an equally important role.