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Viruses with RNA Genomes01:29

Viruses with RNA Genomes

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RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
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Glucose and glutamine drive hepatitis E virus replication.

Shaheen Khan1, Suruchi Aggarwal2, Pooja Bhatia1

  • 1Virology Section, Department of Life Sciences, Shiv Nadar Institution of Eminence, Gautam Buddha Nagar, Greater Noida, UP201314, India.

Archives of Virology
|October 30, 2024
PubMed
Summary
This summary is machine-generated.

Hepatitis E virus (HEV) replication depends on host cell glucose and glutamine metabolism, particularly the hexosamine biosynthetic pathway (HBP). Inhibiting glycolysis, glutaminolysis, or HBP components significantly reduces HEV replication.

Keywords:
GlutaminolysisGlycolysisHSP70HSP90Hepatitis E virusHexosamine biosynthetic pathway

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Area of Science:

  • Virology
  • Metabolic Engineering
  • Molecular Biology

Background:

  • Hepatitis E virus (HEV) genotype 1 replication mechanisms are poorly understood due to limited cell culture and animal models.
  • Viruses adapt host carbon metabolism for replication, but HEV's specific metabolic needs remain unclear.

Purpose of the Study:

  • To investigate the metabolic prerequisites for Hepatitis E virus (HEV) genotype 1 replication.
  • To elucidate the role of host cell carbon sources and metabolic pathways in supporting HEV replication.

Main Methods:

  • Utilized mutant HEV RNA libraries to identify replicative ensembles.
  • Assessed the impact of inhibiting glycolysis, glutaminolysis, and the hexosamine biosynthetic pathway (HBP) on HEV replication.
  • Analyzed protein-metabolite pathways and measured HEV RNA and ORF2 expression.

Main Results:

  • HEV replication significantly increases glucose and glutamine utilization.
  • Inhibition of glycolysis and glutaminolysis similarly reduced HEV replication levels.
  • HEV replication requires fructose-6-phosphate and glutamine via the HBP, which stimulates HSP70 expression, crucial for viral replication.

Conclusions:

  • Glucose and glutamine are critical for HEV replication, primarily through the hexosamine biosynthetic pathway (HBP).
  • Targeting glycolysis, glutaminolysis, HBP enzymes, or HSP70 offers potential strategies for controlling HEV infection.