Understanding How COVID-19 and Its Vaccines Can Affect Shingles Risk

Shingles is a reactivation of the varicella zoster virus, the same virus behind chickenpox. The WHO notes the rash usually appears on one side, often as a single stripe of blisters. Pain often appears before the actual rash. So, what is the connection between the COVID booster and shingles? Well, a large Dutch study recently used GP health records and a self-controlled design. It compared the 28 days after each dose with the same person’s remaining observed time outside post-dose windows. 

The authors found no increased risk after the primary series. Yet they did see a small relative increase after a third mRNA dose. At the same time, a 2024 meta-analysis linked COVID infection with a larger shingles risk signal, about 2.16-fold. Numbers like these need two lenses. Relative risk indicates direction; however, absolute risk shows the number of additional cases that appear. This article will look at both, then lay out who should pay the closest attention and what to do if symptoms start.

Shingles is caused by the varicella zoster virus reactivation. After chickenpox, the virus stays dormant in nerve tissue. Years later, it can reactivate and travel along a nerve to the skin. The WHO notes that a rash often appears on one side. It can look like a single stripe of blisters. Pain is common and can start before the rash. Early symptoms can include tingling, itching, burning, or stabbing pain in a small patch. Blisters then cluster in the same area, and crusting follows. CDC describes shingles as a painful rash illness that happens when the virus reactivates in the body. Some people recover in weeks, yet nerve pain can persist. Shingles is not contagious in the way respiratory viruses spread. The WHO explains that shingles itself is not contagious, but the virus can spread to someone who never had chickenpox. That exposure causes chickenpox, not shingles. 

This helps guide household decisions, especially around infants and pregnant people. Risk rises when immune control drops. WHO notes shingles is more common in adults over 50 and in people with weakened immune systems. Immune suppression can come from cancer treatment, immune disorders, or medicines that reduce immune activity. Acute illness, sleep loss, and stress can also shift immune function. Because shingles is reactivation, timing patterns matter. When shingles appear soon after an infection or vaccination, a trigger is plausible. The next step is measuring frequency across large groups. Antiviral treatment works best when started early. A rash near the eye needs urgent care to protect vision and nerves quickly. 

COVID does not contain the varicella zoster virus, so it cannot cause shingles directly. The connection is immune strain during illness. COVID can produce strong inflammation and temporary immune disruption. Some people develop low lymphocyte counts during acute infection, and recovery can take time. That strain can open a window for dormant viruses to reactivate. GoodRx explains the idea plainly. COVID illness can weaken the immune system and give the virus a chance to wake up and cause shingles. That statement is not a promise for any one person. It describes a pathway that matches how shingles behaves. The strongest evidence comes from pooled studies. A 2024 systematic review and meta-analysis reported results after pooling studies. 

People infected with COVID had a 2.16-fold increased risk of herpes zoster compared with uninfected individuals. The estimate has wide confidence limits, which signal uncertainty, yet it still suggests an association. The same review did not find a significant association between COVID vaccination and shingles when results were pooled. The pooled relative risk for vaccination was 1.08, and the confidence interval crossed 1.0. That does not erase signals from single datasets, but it sets expectations. For real decisions, infection is the proper comparator. Preventing COVID can reduce severe outcomes and may also reduce shingles risk linked to illness. Vaccination changes infection risk. CDC says people up to date have a lower risk of severe illness, hospitalization, and death.WHO says protection against severe disease is highest in the early months. It then decreases, supporting booster timing for higher-risk adults. 

What the Dutch study did

The Dutch study is the central evidence for the COVID booster and shingles. It analysed GP consultations for herpes zoster after COVID-19 vaccination using electronic health record data from Dutch general practices. Participants were aged 12 years and older and had at least one COVID vaccination recorded in 2021. They were registered in the PHARMO GP database or the Nivel Primary Care Database. Vaccination records came from the national register, CIMS, which includes people who consented to data sharing. The authors estimate athat bout 6% of vaccinated Dutch people did not consent. The design was a retrospective self-controlled cohort. Each person served as the comparison for themselves over time. The exposed risk period was the 28 days after each vaccination. The control period was the person’s remaining follow-up time. Poisson regression produced incidence rate ratios, and models adjusted for SARS-CoV-2 infection. 

People with a GP consultation for herpes zoster in the previous 5 years, from 2016 to 2020, were excluded. That reduced bias from recurrent episodes and improved clarity about new consultations. Self-controlled designs reduce confounding from stable traits, such as genetics or long-term illness. They can still be influenced by time-varying behaviour, such as booking a GP visit sooner after vaccination. The paper’s value is scale and timing precision, with more than 2 million vaccinated people in one health system. The authors also tested effect modification. They stratified results by age groups: 12 – 18, 19 – 39, 40 – 59, and 60 or older. They stratified by sex to see risk differed across subgroups. It helps interpret signals with less guesswork.

What it found 

The cohort included 2,098,683 vaccinated people aged 12 years and older. Of these, 1,058,646 were female, which is 50.4%. The outcome was a GP consultation for herpes zoster, a practical marker of clinically recognised cases in primary care. Across all doses and all vaccine types grouped together, the adjusted incidence rate ratio was 1.07. The 95% confidence interval was 1.02 to 1.13. This reflects a 7% relative increase during the 28-day post-vaccination window. The larger signal appeared after dose 3. For the third dose across all vaccines, the adjusted incidence rate ratio was 1.21. The 95% confidence interval was 1.05 to 1.38. This is a relative increase in a short window, not a statement about long-term risk.

When analysis was restricted to mRNA vaccines, results were similar. All mRNA doses grouped had an adjusted incidence rate ratio of 1.06. The confidence interval was 1.00 to 1.12. The third mRNA dose had an adjusted incidence rate ratio of 1.21. The confidence interval was 1.05 to 1.40. The authors describe the overall pattern as a slightly increased risk when all doses are combined. After stratification, they report no increased risk after the primary series. They report a slightly elevated risk after the third or booster mRNA dose. One nuance shapes interpretation. In this dataset, the third dose included people who received three mRNA doses. No one received three vector doses. When the mRNA analysis was split by brand, the increased risk was no longer significant for Pfizer BioNTech. 

Brands and subgroups

The paper does not treat all people as identical. It stratified the results by vaccine type, vaccine brand, age group, and sex. That helps test whether a signal is broad or concentrated. After stratification by vaccine type, the booster signal sat within mRNA vaccination. For vector vaccines, the overall picture was less consistent. The third-dose analysis did not apply because there were no three-dose vector recipients. The most striking subgroup finding involved male individuals and vector vaccines. For males of all ages, the adjusted incidence rate ratio after vector vaccines was 1.38. The 95% confidence interval was 1.02 to 1.87. For mRNA vaccines, sex-stratified estimates were not significant. After further splitting by age categories, the authors report no significant effects in most subgroups. 

Small counts can distort subgroup results. The figures show blank cells where counts were below 5, which signals sparse data. Sparse data widens confidence intervals and makes chance findings more likely. This is not a reason to ignore subgroup work. It is a reason to treat subgroup signals as leads. The brand-level note about Pfizer is an example. After splitting mRNA vaccines by brand, significance disappeared for Pfizer BioNTech.That detail is relevant because Pfizer remained in use in later Dutch campaigns, according to the authors. For clinicians, the takeaway is targeted conversation. A person who is older, male, or immunocompromised may want a plan for shingles symptoms after vaccination. Yet the data do not support assuming everyone faces the same increase. 

The Dutch study reports incidence rate ratios, which are relative measures. Relative risk answers one question. Was shingles more common in the 28 days after vaccination than at other times for the same person? It does not directly answer how many extra cases occurred. Absolute risk depends on baseline shingles rates and the size of the exposed window. Here, the window is 28 days. For many adults under 50, the baseline incidence in a single month is low. A 21% relative rise on a low baseline can still create a few extra cases. Absolute risk rises with age and immune suppression. WHO notes shingles is more common in adults over 50 and in people with weakened immune systems. That means the same relative shift can translate to more cases in older groups, even if the ratio is similar.

Outcome definition also shapes numbers. The study counted GP consultations, not laboratory-confirmed infections. If people seek care sooner after a vaccine, the measured incidence can rise during the risk window. That behaviour effect can inflate estimates, even when biology is unchanged. The self-controlled design reduces confounding from stable personal traits. It does not remove time-linked factors, like a winter surge in appointments or heightened symptom awareness after vaccination. Confidence intervals help, but they do not solve every bias. A balanced reading keeps both measures on the table. Relative risk shows direction. Absolute risk explains the practical impact for real people. Another anchor is exposure likelihood. A booster is a single event, but infection risk can persist for months during waves locally.

Infection is the benchmark 

Any booster discussion needs the infection benchmark. A 2024 systematic review looked at COVID infection. It linked infection with a 2.16-fold increased herpes zoster risk versus no infection. That relative shift is larger than the 1.21 signal. That signal followed a third mRNA dose in the Dutch study.COVID infection also brings risks that shingles data cannot capture. CDC’s COVID-19 vaccine information statement says people who are up to date have a lower risk of severe illness. It notes lower hospitalization and death risk than people not up to date.WHO explains that protection against severe disease and death is highest in the first months after vaccination. It then starts to decrease. Those facts help explain why booster timing focuses on higher-risk adults.

None of this denies the Dutch booster signal. It sets scale and prevents overreaction. A modest, time-bound shingles signal can exist, and infection can still be a larger shingles trigger at the population level. For older adults, both risks rise together. WHO notes shingles is more common in adults over 50. Severe COVID risk also rises with age, so prevention choices often stack. That combination supports a dual plan that reduces infection risk while also lowering reactivation risk. CDC’s 2025–2026 guidance frames vaccination as individual decision-making. It says vaccination is a safer, more reliable way to build protection than getting sick with COVID. For people who face frequent exposure, the infection risk can recur across months. That repeated exposure can outweigh a one-time post-booster window even when booster effects stay rare. 

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Prevention and action 

Risk can be reduced from both angles. One angle is shingles prevention. CDC recommends 2 doses of Shingrix separated by 2 to 6 months for immunocompetent adults aged 50 years and older.CDC also recommends two doses for adults aged 19 years and older. This includes those immunodeficient or immunosuppressed because of disease or therapy. For eligible adults, shingles vaccination lowers baseline reactivation risk. That reduces absolute risk in any short post-booster window. It also reduces the chance of complications such as persistent nerve pain. The second angle is COVID risk reduction. CDC’s 2025 – 2026 guidance recommends vaccination for people 6 months and older using individual decision-making. It states vaccination is a safer way to build protection than getting sick. For people at higher risk, boosters can reduce severe outcomes during waves. 

If shingles symptoms start, early care helps. WHO describes a one-sided rash, often as a stripe of blisters, with pain. Health.com notes shingles is treatable with antivirals. It also notes reports after vaccination show correlation, not proof of cause. A rash near the eye needs urgent evaluation, because vision can be threatened. After recovery, scheduling can be tailored. People on immunosuppressant medicines can coordinate timing with clinicians. People with prior shingles can discuss Shingrix eligibility and future COVID booster timing. The goal is practical prevention, not panic. Keeping a simple timeline can help. Note the vaccine date, first pain date, and rash date. That record helps clinicians decide antiviral windows and report events accurately in pharmacovigilance systems. 

Bottom line 

The Netherlands Drug Safety study offers a clear anchor for the COVID booster and shingles. It used a self-controlled design. It compared the 28 days after vaccination with each person’s other time, adjusting for SARS-CoV-2 infection. The study found a slight increase when all doses and vaccine types were grouped. The adjusted incidence rate ratio was 1.07. It also found a higher signal after a third dose. The adjusted incidence rate ratio was 1.21. In this dataset, third doses were mRNA doses, and brand-level stratification removed significance for Pfizer BioNTech.Those figures describe relative risk in a short window. They do not show that shingles becomes common after boosters. 

Absolute risk still depends on age and immune status, and shingles is more common after age 50. The infection benchmark stays important. A 2024 systematic review linked COVID infection with about a 2.16-fold shingles risk increase. Vaccination also reduces severe COVID outcomes, according to the CDC’s vaccine information statement. A practical approach stacks protections. Eligible adults can reduce shingles risk with a 2-dose Shingrix series.COVID vaccination decisions can then focus on exposure and severe-disease risk, without treating shingles headlines as destiny. If shingles symptoms appear after infection or vaccination, seek care early, especially for rash near the eye. Keeping the discussion anchored to relative and absolute risk prevents fear-based choices. It supports decisions that fit personal health history well. 

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