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Related Concept Videos

Regulation of Nuclear Protein Sorting01:45

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Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
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In Vitro Transcribed RNA-based Luciferase Reporter Assay to Study Translation Regulation in Poxvirus-infected Cells
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Let-7f-5p Inhibits PRRSV Replication by Regulating Lipid Metabolic Reprogramming in Infected Cells.

Dongfeng Jiang1,2, Jin Huang1, Xiaotong Wang1

  • 1College of Animal Science and Technology, Henan University of Animal Husbandry and Economy, Zhengzhou 450046, China.

Veterinary Sciences
|December 31, 2025
PubMed
Summary
This summary is machine-generated.

Porcine reproductive and respiratory syndrome virus (PRRSV) manipulates host lipid metabolism for replication. The microRNA let-7f-5p inhibits PRRSV by reducing lipid accumulation and suppressing viral protein expression, offering a potential antiviral strategy.

Keywords:
PRRSVSREBP2let-7f-5plipid metabolismpig

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Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Lipids are crucial for viral replication and infection.
  • The interplay between lipid metabolism and PRRSV proliferation is not well understood.

Purpose of the Study:

  • To investigate the impact of PRRSV infection on host lipid metabolism.
  • To explore the role of let-7f-5p in modulating lipid metabolism and PRRSV replication.

Main Methods:

  • Transcriptomics, lipidomics, BODIPY staining, Western blot (WB), and quantitative reverse transcription PCR (qRT-PCR).
  • Analysis of lipid metabolism-associated genes and metabolites in PRRSV-infected cells.
  • Investigation of let-7f-5p effects on lipid droplets and viral protein expression.

Main Results:

  • PRRSV infection altered lipid metabolism genes and metabolites, increasing intracellular lipid droplets and upregulating SREBP2.
  • Let-7f-5p reduced lipid droplet accumulation and suppressed PRRSV N protein expression.
  • Fifteen upregulated lipid species were downregulated by let-7f-5p, impacting phosphatidylcholine and fatty acid metabolism pathways.

Conclusions:

  • PRRSV hijacks host lipid metabolism to promote viral replication.
  • Let-7f-5p exhibits antiviral effects against PRRSV through dual mechanisms, targeting lipid metabolism and viral protein synthesis.
  • Modulating host lipid metabolism presents a potential host-directed antiviral strategy against PRRSV.