Rotavirus exploits SREBP pathway for hyper lipid biogenesis during replication.
J Gen Virol
; 103(5)2022 05.
Article
en En
| MEDLINE
| ID: mdl-35594141
ABSTRACT
Species A rotavirus (RVA) is one of the pathogens causing severe acute gastroenteritis in young children and animals worldwide. RVA replicates and assembles its immature particle within electron dense compartments known as viroplasm. Despite the importance of lipid droplet (LD) formation in the RVA viroplasm, the upstream molecules modulating LD formation have remained elusive. Here, we demonstrate that RVA infection reprogrammes sterol regulatory element binding proteins (SREBPs)-dependent lipogenic pathways in virus-infected cells. Interestingly, silencing of SREBPs significantly reduced RVA protein synthesis, genome replication and progeny virus production. Moreover, knockout of SREBP-1c gene conferred resistance to RVA-induced diarrhoea, reduction of RVA replication, and mitigation of small intestinal pathology in mice. This study identifies SREBPs-mediated lipogenic reprogramming in RVA-infected host cells for facilitating virus replication and SREBPs as a potential target for developing therapeutics against RVA infection.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Infecciones por Rotavirus
/
Rotavirus
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Gen Virol
Año:
2022
Tipo del documento:
Article