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Hepatitis C virus hijacks P-body and stress granule components around lipid droplets

Yasuo Ariumi1, Misao Kuroki, Yukihiro Kushima

  • 1Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811, Japan. ariumi@kumamoto-u.ac.jp

Journal of Virology
|May 6, 2011
PubMed

Insights

Hepatitis C virus (HCV) infection disrupts cellular P-bodies and stress granules, hijacking their components for viral replication. Knockdown of these components significantly reduces HCV RNA accumulation, highlighting their essential role in the viral life cycle.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • MicroRNA (miRNA) pathways, including the roles of miR-122 and miRNA effectors like DDX6, are crucial for Hepatitis C Virus (HCV) replication.
  • P-bodies and stress granules are cellular structures involved in mRNA regulation and stress response.

Purpose of the Study:

  • To investigate the impact of HCV-JFH1 infection on P-body and stress granule formation and dynamics.
  • To determine if these cellular components are essential for HCV replication.

Main Methods:

  • Utilized HuH-7-derived RSc cells for HCV-JFH1 infection studies.
  • Observed the dynamic redistribution of miRNA effectors (DDX6, Lsm1, Xrn1, PATL1, Ago2) and stress granule components (G3BP1, ATX2, PABP1) using microscopy.
  • Performed knockdown experiments for DDX6, Lsm1, ATX2, and PABP1 to assess their role in HCV RNA accumulation.
  • Investigated the effect of HCV infection on stress granule formation under induced stress conditions (heat shock, arsenite).

Main Results:

  • HCV-JFH1 infection disrupted P-body formation and redistributed miRNA effectors and stress granule components to sites of viral production around lipid droplets.
  • Disruption of P-body formation and redistribution of components occurred at late stages of infection (≥36-48 hours post-infection).
  • HCV infection suppressed stress granule formation in response to cellular stress.
  • Knockdown of DDX6, Lsm1, ATX2, and PABP1 significantly reduced HCV RNA accumulation, indicating their necessity for viral replication.

Conclusions:

  • HCV hijacks P-body and stress granule components, essential for its replication.
  • Disruption of P-bodies and recruitment of their components to viral factories are key events in the late stage of HCV infection.
  • Targeting these cellular components could represent a novel therapeutic strategy against HCV.

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