SCHMIDT, Katarina Wendy; MONTESPAN, Charlotte; THOMPSON, Danielle; LUCAS, Miriam S; LIGEON, Laure-Anne; WODRICH, Harald; HAHN, Alexander S; GREBER, Urs F; MÜNZ, Christian

doi:10.1016/j.celrep.2024.115019

Métadonnées

Afficher la notice complète

Licence d’utilisation du document

SCHMIDT, Katarina Wendy

MONTESPAN, Charlotte

THOMPSON, Danielle

Langue

Article de revue

Ce document a été publié dans

Cell Reports. 2024-11-26, vol. 43, n° 12, p. 115019

Résumé en anglais

Kaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic γ-herpesvirus. Autophagy during KSHV entry has remained unexplored. We show that LC3 lipidation as a hallmark of autophagy is induced shortly after KSHV entry. LC3 co-localizes with KSHV in amphisomes during entry and loss of LC3 lipidation increases infection. Accordingly, NDP52, a receptor of selective autophagy, was recruited to endocytosed viral particles, and its reduction increased KSHV infection. Additionally, virus particles co-localized with the endolysosome damage sensor galectin-8 upon KSHV entry and depletion of galectin-8 promoted KSHV infection. Compared with herpes simplex virus, listeriolysin, adenovirus, and influenza virus, and in contrast to what was previously thought about enveloped viruses, KSHV binding to EphA2 by its envelope protein gH causes endolysosomal membrane damage, akin to non-enveloped viruses and bacteria. Taken together, our study identifies an important anti-viral role for galectin-8, NDP52, and the autophagy machinery at virus-damaged endosomes, restricting KSHV entry by selective autophagy.< Réduire

Métadonnées

Partager cette publication !

Licence d’utilisation du document

Selective autophagy impedes KSHV entry after recruiting the membrane damage sensor galectin-8 to virus-containing endosomes.

Langue

Ce document a été publié dans

Résumé en anglais

URI

DOI

Unités de recherche