Exosome mimicry by a HAVCR1-NPC1 pathway of endosomal fusion mediates hepatitis A virus infection.

ABSTRACT: Cell-to-cell communication by exosomes controls normal and pathogenic processes^1,2. Viruses can spread in exosomes and thereby avoid immune recognition³. While biogenesis, binding and uptake of exosomes are well characterized^4,5, delivery of exosome cargo into the cytoplasm is poorly understood³. We report that the phosphatidylserine receptor HAVCR1 (refs. ^6,7) and the cholesterol transporter NPC1 (ref. ⁸) participate in cargo delivery from exosomes of hepatitis A virus (HAV)-infected cells (exo-HAV) by clathrin-mediated endocytosis. Using CRISPR-Cas9 knockout technology, we show that these two lipid receptors, which interact in the late endosome⁹, are necessary for the membrane fusion and delivery of RNA from exo

SUBMITTER: Costafreda MI 

PROVIDER: S-EPMC7483988 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature