Shingles, also known as herpes zoster, is a viral infection that causes a painful rash and blisters. It is caused by the varicella-zoster virus, the same virus that causes chickenpox. After a person recovers from chickenpox, the virus remains dormant in the body. Years later, it can reactivate as shingles. Besides the rash and pain, shingles can lead to serious complications, especially in people with weakened immune systems. One such complication is the development or exacerbation of autoimmune diseases.
What are autoimmune diseases?
Autoimmune diseases occur when the immune system mistakenly attacks the body’s own healthy cells and tissues. This can lead to inflammation, damage, and dysfunction of various body systems. Some common autoimmune diseases include rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, inflammatory bowel disease, psoriasis, Hashimoto’s thyroiditis, and more. It is not entirely clear why some people develop autoimmune diseases, but risk factors include family history, environmental exposures, infections, hormonal influences, and stress.
How shingles can trigger autoimmune diseases
The varicella-zoster virus has an intriguing relationship with the immune system. After the initial chickenpox infection, the virus can hide out in nerve cells and remain dormant for decades. When the immune system is weakened, the virus can reactivate to cause shingles. Research shows that a shingles infection can damage the immune system and make people more susceptible to developing autoimmune diseases. Here are some of the ways this may occur:
- The varicella-zoster virus infects and destroys T cells, which are important immune cells that normally help regulate the immune response. Loss of these cells can impair immunity and allow autoimmune reactions to develop.
- Viral replication during shingles leads to the release of large amounts of viral particles, proteins, and DNA that the immune system reacts to. This overstimulation of the immune system can lead it to misidentify the body’s own cells as foreign threats.
- The cell damage caused by the shingles infection exposes intracellular proteins and other molecules that are normally hidden from the immune system. The immune system may produce antibodies against these newly exposed components that also react against normal tissues and trigger autoimmunity.
- Shingles can induce localized inflammation in affected dermatomes that spreads systemically. This inflammation can damage tissues and sustain autoimmune reactions.
- Some research suggests that the varicella-zoster virus has proteins that mimic normal human proteins. This molecular mimicry can confuse the immune system and allow autoimmune reactions to develop.
The net result is that the chaos induced by a shingles infection can disrupt immune tolerance and activate pathogenic immune cells that initiate and propagate autoimmune diseases in genetically susceptible individuals.
Autoimmune diseases associated with shingles
Several autoimmune disorders have been clinically associated with shingles infections. Some of the main ones include:
Rheumatoid Arthritis
Rheumatoid arthritis (RA) causes joint swelling, pain, and eventual deformity. It results from the immune system attacking the synovial membranes that line joints. Multiple studies show an increased risk of developing RA after having shingles. In one study, the risk of RA was >4 times higher in shingles patients compared to controls without shingles. The autoimmune processes are thought to be triggered by viral exposure and replication in joint tissues.
Multiple Sclerosis
Multiple sclerosis (MS) is an autoimmune disease where the immune system attacks the myelin sheath that insulates nerves. This leads to neurological impairments. Research indicates that a history of shingles increases the likelihood of developing MS. It is theorized that immune cells primed by the shingles virus cross-react with myelin basic protein in the central nervous system.
Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is a multi-system autoimmune disorder that can affect the joints, skin, kidneys, and other organs. Studies demonstrate that patients with SLE have a higher seroprevalence of varicella-zoster virus antibodies compared to controls without SLE. Shingles infections are also associated with SLE flares. The virus is thought stimulate aberrant immune responses against nuclear antigens through molecular mimicry mechanisms.
Type 1 Diabetes
Type 1 diabetes results from destruction of the insulin-producing beta cells in the pancreas by autoimmune T cells and antibodies. Case reports have documented the onset of type 1 diabetes in children following varicella and herpes zoster virus infections. Virus-induced inflammation in the pancreas is believed to activate autoimmune lymphocytes that target pancreatic islet cells.
Autoimmune Thyroid Diseases
Hashimoto’s thyroiditis is an autoimmune disorder involving the thyroid gland. Rare cases of Hashimoto’s diagnosed after a shingles infection have been reported. There is also an epidemiological association between shingles and increased risk of Graves’ disease, another autoimmune thyroid condition. The suspected mechanism is molecular mimicry between viral antigens and thyroid proteins.
Inflammatory Bowel Diseases
Inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis are characterized by chronic intestinal inflammation. IBD flares have been documented in patients following shingles infections. It is hypothesized that the shingles virus damages the gastrointestinal mucosa and elicits an aggressive autoimmune reaction mediated by infiltrating lymphocytes and antibodies.
Other Autoimmune Diseases
There are also cases reports linking new-onset autoimmune diseases such as autoimmune hemolytic anemia, Guillain-Barre syndrome, and IgA nephropathy to prior herpes zoster viral infections. The associations are not fully proven, but shingles likely plays a contributing role in provoking these autoimmune conditions in predisposed individuals.
Risk Factors
Not everyone who gets shingles will develop a secondary autoimmune illness. There are some risk factors that increase susceptibility:
- Genetic predisposition – Having genes linked to autoimmunity raises the risk.
- Older age – The elderly are more prone to autoimmunity after shingles.
- Repeated shingles infections – Multiple bouts place greater stress on the immune system.
- Immunosuppression – Weakened immune defenses are more vulnerable to dysregulation.
- Extent of viral replication – Higher viral loads potentially drive greater autoimmunity.
- Slow clearance of virus – Persistent viral antigens can prolong immune stimulation.
The location of the shingles rash may also influence which autoimmune condition develops. For example, facial shingles infections have been associated with a higher risk of subsequent giant cell arteritis.
Prevention and Treatment
Since shingles can lead to serious autoimmune complications, especially in high-risk groups, it is important to prevent shingles in the first place. The shingles vaccine is recommended for healthy adults age 50 and older to boost immunity against the virus. Some additional strategies include:
- Early antiviral treatment at the first sign of shingles to limit viral load and damage
- Prompt pain control to minimize inflammation
- Stress management to limit immune impairment
- Avoiding immunosuppressive drugs when possible
- Careful monitoring after shingles for signs of new autoimmune activity
For those who develop an autoimmune disease following shingles, conventional treatments like steroids, immunosuppressants, and monoclonal antibodies can help calm the overactive immune response. But medications may need to be adjusted in those already taking them for shingles or other conditions. Long term, rebuilding immune tolerance through approaches like IVIG, plasmapheresis, and stem cell transplants may help reset the immune system and prevent further autoimmune damage.
The Bottom Line
In summary, the varicella-zoster virus that causes shingles has been linked to several autoimmune disorders including rheumatoid arthritis, multiple sclerosis, lupus, type 1 diabetes, thyroid disease, and inflammatory bowel disease. The virus likely triggers these conditions through a combination of immune stimulation, inflammation, molecular mimicry, and tissue damage. Those at highest risk include older adults, the immunosuppressed, and those with genetic predisposition. Preventing shingles with vaccination and controlling viral damage and inflammation during active infections are important to limit complications. Increased awareness and monitoring for autoimmune diseases after shingles can allow for early intervention. Ongoing research is still needed to fully understand the complex interplay between viral infections like shingles and autoimmunity.