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Rotavirus exploits SREBP pathway for hyper lipid biogenesis during replication.

Ahsan Naveed1, Muhammad Ammar Naveed2, Lubna Akram2

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The Journal of General Virology
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Species A rotavirus (RVA) infection reprograms host cell lipid pathways. Targeting sterol regulatory element binding proteins (SREBPs) inhibits RVA replication and may offer new therapeutic strategies.

Keywords:
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Area of Science:

  • Virology
  • Molecular Biology
  • Host-Pathogen Interactions

Background:

  • Species A rotavirus (RVA) causes severe gastroenteritis globally in children and animals.
  • Viroplasm, the site of RVA replication, involves lipid droplet (LD) formation, but upstream regulators remain unclear.

Purpose of the Study:

  • To investigate the role of sterol regulatory element binding proteins (SREBPs) in RVA-induced lipid droplet formation and viral replication.
  • To identify SREBPs as potential therapeutic targets for RVA infection.

Main Methods:

  • Investigated SREBP-dependent lipogenic pathways in RVA-infected cells.
  • Utilized gene silencing (siRNA) to assess the impact of SREBPs on RVA replication.
  • Generated SREBP-1c knockout mice to evaluate in vivo resistance to RVA.

Main Results:

  • RVA infection reprogrammes SREBP-dependent lipogenic pathways.
  • SREBP silencing significantly reduced RVA protein synthesis, genome replication, and progeny virus production.
  • SREBP-1c knockout mice showed resistance to RVA-induced diarrhea, reduced viral replication, and mitigated intestinal pathology.

Conclusions:

  • SREBPs mediate lipogenic reprogramming in host cells, facilitating RVA replication.
  • SREBPs represent a promising therapeutic target for combating rotavirus infections.