| Literature DB >> 29196796 |
Pieter Meysman1,2,3, Nicolas De Neuter4,5,6, Esther Bartholomeus6,7,8, George Elias6,9,10, Johan Van den Bergh9, Marie-Paule Emonds11, Geert W Haasnoot12, Steven Heynderickx9,10, Johan Wens13, Nele R Michels13, Julien Lambert14, Eva Lion9,10, Frans H J Claas12, Herman Goossens15,16, Evelien Smits6,9,10,17, Pierre Van Damme18, Viggo Van Tendeloo6,9, Philippe Beutels6,19,20, Arvid Suls6,7,8, Geert Mortier6,7,8, Kris Laukens4,5,6, Benson Ogunjimi6,9,19,21,22.
Abstract
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.Entities:
Keywords: HLA association; Herpes zoster; MHC peptide affinity; Varicella zoster virus
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Year: 2017 PMID： 29196796 DOI： 10.1007/s00251-017-1047-x
Source DB: PubMed Journal: Immunogenetics ISSN： 0093-7711 Impact factor: 3.330