Can COVID-19 (Coronavirus Disease 2019) trigger shingles, particularly in individuals with weakened immune systems or chronic medical conditions?

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COVID-19 and Shingles Reactivation

Yes, COVID-19 infection can trigger shingles (herpes zoster) reactivation, particularly in individuals aged 50 years and older, and this association is supported by multiple large cohort studies showing statistically significant increased risk following SARS-CoV-2 infection. 1, 2

Mechanism of VZV Reactivation

The biological basis for shingles reactivation following COVID-19 relates to immune dysfunction:

  • SARS-CoV-2 infection produces an immunosuppressive state characterized by T cell dysfunction, including lymphopenia and lymphocyte exhaustion, which favors varicella zoster virus (VZV) reactivation 1, 2

  • COVID-19 causes transient but significant impairment of cell-mediated immunity, specifically affecting the VZV-specific T-cell responses that normally keep the latent virus suppressed 2, 3

  • The virus induces a biphasic immune response: early immunosuppression allowing viral replication, followed by potential hyperinflammation ("cytokine storm") in severe cases 4

Evidence from Large Population Studies

Three major cohort studies provide the strongest evidence:

  • A multinational study, along with large US and Spanish cohorts, reported significantly increased risk of herpes zoster following COVID-19 infection, with the effect most pronounced in people aged ≥50 years 1

  • These studies specifically excluded individuals vaccinated against herpes zoster, strengthening the causal inference 1

  • One Israeli study that did not account for HZ vaccination status found no increase, highlighting the importance of study design in detecting this association 1

Clinical Presentation and Timing

Typical characteristics of COVID-19-associated shingles:

  • Herpes zoster most frequently occurs within 1-2 weeks of COVID-19 infection 2

  • The majority of cases present with typical dermatomal distribution 2

  • Atypical presentations occur more commonly in patients with lymphopenia, suggesting more severe immune compromise 2

  • Twenty-seven documented cases have been reported in the literature, though this likely represents significant underreporting 2

High-Risk Populations

Individuals at greatest risk for COVID-19-triggered shingles include:

  • Older adults (≥50 years) who have age-related decline in VZV-specific immunity 1, 2

  • Patients with pre-existing immunosuppressive conditions including cancer, autoimmune diseases, or chronic organ disease 4, 2

  • Those with chronic medical comorbidities such as diabetes, cardiovascular disease, or chronic kidney disease 4

  • Individuals on immunosuppressive medications, particularly those affecting T-cell function 4

COVID-19 Vaccination and Shingles Risk

The relationship between COVID-19 vaccination and shingles is more nuanced:

  • Some large analyses have reported a statistically significant association between mRNA COVID-19 vaccines and herpes zoster development, including studies from Israel, Hong Kong, and the US VAERS database 1

  • A real-world study of over 1 million vaccinated individuals found a risk ratio of 1.802 (95% CI 1.680-1.932) for developing shingles within 60 days post-vaccination compared to unvaccinated controls 5

  • The absolute risk remains low: 0.20% in vaccinated versus 0.11% in unvaccinated individuals 5

  • The mechanism may involve transient lymphocytopenia similar to that seen in COVID-19 infection itself 3

  • This phenomenon varies by vaccine type, with most cases (86.27%) reported following mRNA vaccines 6

  • 80% of herpes zoster cases occurred after the first (priming) dose among mRNA vaccine recipients 6

Critical Context and Clinical Implications

Important caveats for clinical practice:

  • VZV reactivation is not COVID-19-specific—it is a well-established phenomenon with other infections and vaccines 5

  • The benefits of COVID-19 vaccination vastly outweigh the small risk of shingles reactivation 1

  • Disruption of routine shingles vaccination programs during the pandemic resulted in an estimated 63,117 avoidable herpes zoster cases in the USA alone 1

  • Practitioners should maintain heightened awareness for shingles during and after COVID-19 infection, particularly in older adults and immunocompromised patients 2

  • Early recognition and treatment with antivirals (acyclovir, valacyclovir, or famciclovir) within 72 hours of rash onset is critical to prevent complications 2

Preventive Recommendations

To mitigate shingles risk in the COVID-19 era:

  • Ensure age-appropriate herpes zoster vaccination (Shingrix preferred for adults ≥50 years) is up to date, particularly now that routine vaccination services have resumed 1

  • Consider prophylactic antiviral therapy in high-risk immunocompromised patients during acute COVID-19 infection, though this is not standard practice and requires individual risk-benefit assessment 2

  • Maintain vigilance for early signs of shingles (prodromal pain, dermatomal rash) in patients recovering from COVID-19 2

  • Do not delay COVID-19 vaccination due to concerns about shingles risk—the absolute risk is small and the protection against severe COVID-19 is paramount 1

References

Research

Herpes zoster after COVID vaccination.

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases, 2021

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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