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A combined proteomics/genomics approach links hepatitis C virus infection with nonsense-mediated mRNA decay

Holly R Ramage1,2, G Renuka Kumar1,2, Erik Verschueren2,3

  • 1Gladstone Institutes, 1650 Owens Street, San Francisco, CA 94158, USA.

Molecular Cell
|January 24, 2015
PubMed

Insights

Hepatitis C virus (HCV) infection disrupts host cell functions by altering protein interactions, particularly involving mitochondrial proteins and the nonsense-mediated mRNA decay pathway. This study maps key interactions to reveal how HCV perturbs cellular mechanisms.

Area of Science:

  • Virology
  • Molecular Biology
  • Hepatology

Background:

  • Hepatitis C virus (HCV) is a major cause of liver disease.
  • Understanding virus-host interactions is crucial for developing antiviral strategies.

Purpose of the Study:

  • To comprehensively map host protein interactions for all ten HCV proteins.
  • To identify host factors and pathways disrupted by HCV infection.

Main Methods:

  • Affinity purification coupled with mass spectrometry to identify HCV-host protein-protein interactions.
  • RNA interference (RNAi) screening to assess the functional significance of host interactions.
  • A two-step scoring approach to establish high-confidence interaction networks.

Main Results:

  • A map of 139 high-confidence HCV-host protein-protein interactions was generated.
  • Mitochondrial proteins were identified as significantly involved in HCV infection.
  • HCV core protein interaction with WIBG disrupts the nonsense-mediated mRNA decay pathway, leading to transcript accumulation.

Conclusions:

  • This study provides a detailed map of HCV-host interactions.
  • HCV perturbs host cellular surveillance mechanisms, such as nonsense-mediated mRNA decay, to facilitate infection.
  • These findings offer insights into HCV pathogenesis and potential therapeutic targets.

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