Language

English

Publication Date

12-19-2023

Journal

Proceedings of the National Academy of Sciences of the United States of America

DOI

10.1073/pnas.2302161120

PMID

38079544

PMCID

PMC10743370

PubMedCentral® Posted Date

12-11-2023

PubMedCentral® Full Text Version

Post-print

Abstract

Gastroenteritis is among the leading causes of mortality globally in infants and young children, with rotavirus (RV) causing ~258 million episodes of diarrhea and ~128,000 deaths annually in infants and children. RV-induced mechanisms that result in diarrhea are not completely understood, but malabsorption is a contributing factor. RV alters cellular lipid metabolism by inducing lipid droplet (LD) formation as a platform for replication factories named viroplasms. A link between LD formation and gastroenteritis has not been identified. We found that diacylglycerol O-acyltransferase 1 (DGAT1), the terminal step in triacylglycerol synthesis required for LD biogenesis, is degraded in RV-infected cells by a proteasome-mediated mechanism. RV-infected DGAT1-silenced cells show earlier and increased numbers of LD-associated viroplasms per cell that translate into a fourfold-to-fivefold increase in viral yield (

Keywords

Child, Infant, Humans, Child, Preschool, Rotavirus, Diacylglycerol O-Acyltransferase, Virus Replication, Gastroenteritis, Diarrhea, Rotavirus Infections, rotavirus, DGAT1, lipid droplet, viroplasm, proteasome degradation

Published Open-Access

yes

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