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RNR-R2 Upregulation by a Short Non-Coding Viral Transcript.

Karin Broennimann1, Inna Ricardo-Lax1,2, Julia Adler1

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Biomolecules
|December 24, 2021
PubMed
Summary
This summary is machine-generated.

Hepatitis B virus (HBV) replication in non-dividing cells is supported by a non-coding RNA element, ERE, which activates the DNA damage response (DDR) pathway to increase dNTPs, independent of HBx protein production.

Keywords:
Hepatitis B virusRNR-R2 regulationdeoxynucleotides and DNA virusesnon-coding RNA

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Area of Science:

  • Virology
  • Molecular Biology
  • Hepatitis B Virus Research

Background:

  • DNA viruses need deoxynucleotide triphosphates (dNTPs) for replication.
  • Hepatitis B virus (HBV) replicates in non-dividing cells where dNTPs are scarce.
  • Previous studies indicated HBV induces the DNA damage response (DDR) pathway to increase dNTPs.

Purpose of the Study:

  • To elucidate the mechanism by which HBV induces the DDR pathway and RNR-R2 upregulation.
  • To investigate the role of the HBx protein in this process.
  • To identify the viral component responsible for activating the DDR pathway in non-cycling cells.

Main Methods:

  • Utilized HepG2 cells and primary human hepatocytes.
  • Investigated the function of a conserved region within the HBx open reading frame (ORF).
  • Assessed the impact of an HBV mRNA embedded regulatory element (ERE) on the ATR-Chk1-E2F1-RNR-R2 pathway.

Main Results:

  • HBx protein production is dispensable for inducing the DDR pathway.
  • A 125-base conserved region within the HBx ORF, termed ERE, is sufficient to upregulate RNR-R2 expression.
  • ERE alone activates the ATR-Chk1-E2F1-RNR-R2 DDR pathway in growth-arrested cells.

Conclusions:

  • HBV utilizes a non-coding RNA element (ERE) to enhance viral replication in non-cycling cells.
  • This ERE activates the DDR pathway, increasing dNTP pools independently of HBx protein.
  • Demonstrates a novel non-coding function of HBV transcripts in viral propagation.