ArticleThe Journal of infectious diseases2024
Unraveling the Immune Signature of Herpes Zoster: Insights Into the Pathophysiology and Human Leukocyte Antigen Risk Profile.
Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- The ageing immune system and its battle with viruses.The Journal of general virology · 2026Review
- The impact of personalized nutritional intake on serum inflammation, immune markers, and recovery time in patients with herpes zoster.BMC infectious diseases · 2026Article
- Plasma proteins and herpes simplex virus infection: a proteome-wide Mendelian randomization study.Virus genes · 2025Article
- Loss of tolerance precedes triggering and lifelong persistence of pathogenic type I interferon autoantibodies.The Journal of experimental medicine · 2024Article
- Varicella-zoster virus recapitulates its immune evasive behaviour in matured hiPSC-derived neurospheroids.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
24 authors at 6 institutions in 7 countries.
Funding
Abstract
The varicella-zoster virus (VZV) infects >95% of the population. VZV reactivation causes herpes zoster (HZ), known as shingles, primarily affecting the elderly and individuals who are immunocompromised. However, HZ can occur in otherwise healthy individuals. We analyzed the immune signature and risk profile in patients with HZ using a genome-wide association study across different UK Biobank HZ cohorts. Additionally, we conducted one of the largest HZ human leukocyte antigen association studies to date, coupled with transcriptomic analysis of pathways underlying HZ susceptibility. Our findings highlight the significance of the major histocompatibility complex locus for HZ development, identifying 5 protective and 4 risk human leukocyte antigen alleles. This demonstrates that HZ susceptibility is largely governed by variations in the major histocompatibility complex. Furthermore, functional analyses revealed the upregulation of type I interferon and adaptive immune responses. These findings provide fresh molecular insights into the pathophysiology and activation of innate and adaptive immune responses triggered by symptomatic VZV reactivation.
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Registered trials
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