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Bluetongue virus entry into cells.

Mario Forzan1, Mark Marsh, Polly Roy

  • 1Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1 7HT, United Kingdom.

Journal of Virology
|February 3, 2007
PubMed
Summary
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Bluetongue virus (BTV) enters cells via clathrin-mediated endocytosis. Low pH in early endosomes triggers BTV penetration, revealing its entry mechanism.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Bluetongue virus (BTV), an Orbivirus, possesses a nonenveloped structure with inner and outer capsids.
  • Outer capsid proteins VP2 and VP5 mediate cell entry and core delivery.
  • The precise mechanism of BTV cell entry remains largely uncharacterized.

Purpose of the Study:

  • To elucidate the specific pathway and mechanism of Bluetongue virus entry into host cells.
  • To investigate the role of endocytosis and endosomal pH in BTV infection.

Main Methods:

  • RNA interference (RNAi) was employed to inhibit clathrin-dependent endocytosis.
  • The ATPase inhibitor bafilomycin A1 was used to assess the role of acidic pH.
  • Microscopic analysis was performed on BTV-infected cells.

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Main Results:

  • Inhibition of clathrin-dependent endocytosis significantly reduced BTV internalization and replication.
  • Exposure to acidic pH, facilitated by bafilomycin A1, is essential for productive BTV infection.
  • BTV is internalized into early endosomes, where dissociation of the outer capsid from the inner core occurs.

Conclusions:

  • Bluetongue virus entry is mediated by clathrin-mediated endocytosis from the plasma membrane.
  • BTV penetration into the cytoplasm is triggered by low pH within early endosomes.
  • These findings support a stepwise model for BTV cell entry and penetration.