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Prototype foamy virus downregulates RelB expression to facilitate viral replication.

Junshi Zhang1, Chenchen Wang1, Xiaopeng Tuo1

  • 1Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai University, Tianjin, China.

FEBS Open Bio
|September 4, 2020
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Summary

Prototype foamy virus (PFV) infection downregulates RelB, a cellular factor that restricts viral gene expression. Decreased RelB levels enhance PFV replication by promoting viral promoter activity.

Keywords:
IPLTRRelBprototype foamy virustranscription

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Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Foamy viruses (FVs), subfamily Spumaretrovirinae, exhibit strong in vitro cytopathic effects but establish lifelong latent infections in hosts.
  • The influence of cellular factors on FV replication remains largely uncharacterized.
  • Understanding host-pathogen interactions is crucial for deciphering viral pathogenesis.

Purpose of the Study:

  • To investigate the impact of prototype foamy virus (PFV) infection on host cellular gene expression.
  • To identify cellular factors that modulate PFV replication.
  • To elucidate the mechanism by which PFV interacts with host factors.

Main Methods:

  • Transcriptome analysis of HT1080 cells infected with PFV.
  • Quantitative real-time PCR to validate gene expression changes.
  • Functional studies involving RelB overexpression and small interfering RNA (siRNA)-mediated depletion.

Main Results:

  • PFV infection significantly decreased the mRNA levels of RelB, a nuclear factor-κB (NF-κB) family member.
  • RelB overexpression inhibited PFV replication, while RelB depletion using siRNA enhanced it.
  • RelB's inhibitory effect on PFV is mediated by reduced transactivation of viral promoters (LTR and IP) by the viral Tas protein.

Conclusions:

  • PFV infection actively downregulates the host factor RelB, which normally restricts viral gene expression.
  • RelB acts as a viral inhibitory host factor, limiting PFV replication.
  • This study reveals a novel mechanism of host-pathogen interaction where the virus manipulates a cellular factor to facilitate its own replication.