Increased herpes zoster risk associated with poor HLA-A immediate early 62 protein (IE62) affinity

Pieter Meysman, Nicolas De Neuter, Esther Bartholomeus, George Elias, Johan Van den Bergh, Marie-Paule Emonds, Geert W Haasnoot, Steven Heynderickx, Johan Wens, Nele R Michels, Julien Lambert, Eva Lion, Frans H J Claas, Herman Goossens, Evelien Smits, Pierre Van Damme, Viggo Van Tendeloo, Philippe Beutels, Arvid Suls, Geert MortierKris Laukens, Benson Ogunjimi

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Around 30% of individuals will develop herpes zoster (HZ), caused by the varicella zoster virus (VZV), during their life. While several risk factors for HZ, such as immunosuppressive therapy, are well known, the genetic and molecular components that determine the risk of otherwise healthy individuals to develop HZ are still poorly understood. We created a computational model for the Human Leukocyte Antigen (HLA-A, -B, and -C) presentation capacity of peptides derived from the VZV Immediate Early 62 (IE62) protein. This model could then be applied to a HZ cohort with known HLA molecules. We found that HLA-A molecules with poor VZV IE62 presentation capabilities were more common in a cohort of 50 individuals with a history of HZ compared to a nationwide control group, which equated to a HZ risk increase of 60%. This tendency was most pronounced for cases of HZ at a young age, where other risk factors are less prevalent. These findings provide new molecular insights into the development of HZ and reveal a genetic predisposition in those individuals most at risk to develop HZ.

Original languageEnglish
Pages (from-to)363-372
Number of pages10
Issue number6
Publication statusPublished - Jun 2018


  • Herpes zoster
  • HLA association
  • MHC peptide affinity
  • Varicella zoster virus


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