Immunogenetics · 2017
Increased herpes zoster risk associated with poor HLA-A immediate early 62 protein (IE62) affinity.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Meysman Pieter, De Neuter Nicolas, Bartholomeus Esther, Elias George, Van den Bergh Johan, Emonds Marie-Paule, Haasnoot Geert W, Heynderickx Steven, Wens Johan, Michels Nele R, Lambert Julien, Lion Eva, Claas Frans H J, Goossens Herman, Smits Evelien, Van Damme Pierre, Van Tendeloo Viggo, Beutels Philippe, Suls Arvid, Mortier Geert, Laukens Kris, Ogunjimi Benson
Аннотация
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.