Proceedings of the National Academy of Sciences of the United States of America · 2026
The 4EHP/GIGYF2 translation repressor complex is co-opted by the vaccinia virus K3L protein as a potential mechanism of immunoevasion.
СтатьяНазвание 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.
Ladak Reese Jalal, Pelin Adrian, Zhuang Haotian, Abboud Chelsea, Mahmood Niaz, Blanchet Jonathan, Wu Chenyue, Hoang Huy-Dung, McGirr Tom, Moshari Andia, Moustafa-Kamal Mohamed, Snell Patric Harris, Düsterhöft Stefan, Berghuis Albert M, Trempe Jean-François, Tremblay Michel L, Teodoro Jose G, Khoutorsky Arkady, Alain Tommy, Krogan Nevan J, Choi Jung-Hyun, Jafarnejad Seyed Mehdi, Sonenberg Nahum
Аннотация
Poxviruses have evolved robust immunoevasion strategies to facilitate replication in the cytosol. We previously reported that like several RNA viruses, vaccinia virus replication is impaired in the absence of the host cap-binding translation repressor protein 4EHP (eIF4E2), implicating the latter in host antiviral defense regulation and immunosuppression. Here, we show that the vaccinia virus-encoded K3L protein interacts with 4EHP via its obligatory binding partner GIGYF2 to increase the stability of the 4EHP/GIGYF2 complex. Consequently, K3L bolsters 4EHP/GIGYF2-mediated mRNA translation repression. Thus, we demonstrate that a 4EHP/GIGYF2-mediated mechanism is exploited by and conserved among RNA and DNA viruses as a potential immunoevasion strategy. Our findings document a 4EHP/GIGYF2-dependent stringent regulation of infection by poxviruses, a clinically important family of viruses that are employed as vaccine vectors and in oncolytic viral therapy.