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- W3136012943 abstract "Hepatitis A virus (HAV) is a positive-sense RNA virus causing acute inflammation of the liver. Here, using a genome-scale CRISPR screen, we provide a comprehensive picture of the cellular factors that are exploited by HAV. We identify genes involved in sialic acid/ganglioside biosynthesis and members of the eukaryotic translation initiation factor complex, corroborating their putative roles for HAV. Additionally, we uncover all components of the cellular machinery for UFMylation, a ubiquitin-like protein modification. We show that HAV translation specifically depends on UFM1 conjugation of the ribosomal protein RPL26. Furthermore, we find that components related to the yeast Trf4/5-Air1/2-Mtr4 polyadenylation (TRAMP) complex are required for viral translation independent of controlling viral poly(A) tails or RNA stability. Finally, we demonstrate that pharmacological inhibition of the TRAMP-like complex decreases HAV replication in hepatocyte cells and human liver organoids, thus providing a strategy for host-directed therapy of HAV infection." @default.
- W3136012943 created "2021-03-29" @default.
- W3136012943 creator A5000375474 @default.
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- W3136012943 creator A5059138855 @default.
- W3136012943 creator A5084645336 @default.
- W3136012943 date "2021-03-01" @default.
- W3136012943 modified "2023-10-16" @default.
- W3136012943 title "A genome-wide CRISPR screen identifies UFMylation and TRAMP-like complexes as host factors required for hepatitis A virus infection" @default.
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- W3136012943 doi "https://doi.org/10.1016/j.celrep.2021.108859" @default.
- W3136012943 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33730579" @default.
- W3136012943 hasPublicationYear "2021" @default.
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