4.4 Article

Rotavirus exploits SREBP pathway for hyper lipid biogenesis during replication

期刊

JOURNAL OF GENERAL VIROLOGY
卷 103, 期 5, 页码 -

出版社

MICROBIOLOGY SOC
DOI: 10.1099/jgv.0.001757

关键词

rotavirus; SREBPs; knockout; viroplasm; mice

资金

  1. Basic Science Research Program through the National Research Foundation of Korea - Ministry of Science, ICT and Future Planning, Republic of Korea [2019R1A2C1006502, 2020R1A2B03002517]
  2. National Research Foundation of Korea [2019R1A2C1006502] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

This study identifies the reprogramming of lipogenic pathways in RVA-infected host cells, facilitated by SREBPs, to promote virus replication. SREBPs could be a potential target for developing therapeutics against RVA infection.
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-lc 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.

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