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Related Experiment Videos

Vaccinia virus motility.

Geoffrey L Smith1, Brendan J Murphy, Mansun Law

  • 1Department of Virology, The Wright-Fleming Institute, Faculty of Medicine, Imperial College London, St. Mary's Campus, Norfolk Place, London W2 1PG, United Kingdom. glsmith@imperial.ac.uk

Annual Review of Microbiology
|October 7, 2003
PubMed
Summary
This summary is machine-generated.

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Vaccinia virus (VV) uses host cell microtubules for intracellular movement and actin polymerization for cell-to-cell spread. Different VV particle types facilitate movement within and between hosts.

Area of Science:

  • Virology
  • Cell Biology
  • Microbiology

Background:

  • Vaccinia virus (VV), the causative agent of smallpox vaccine, replicates within the host cell cytoplasm.
  • Efficient intracellular transport of large viruses like VV necessitates specific cellular mechanisms.
  • Understanding VV's movement is crucial for controlling viral spread and pathogenesis.

Purpose of the Study:

  • To elucidate the mechanisms of Vaccinia virus intracellular transport.
  • To investigate the role of microtubules and actin polymerization in VV dissemination.
  • To discuss the function of distinct VV particle forms in host-to-host transmission.

Main Methods:

  • Microscopy techniques to visualize VV movement within infected cells.
  • Analysis of viral protein interactions with host cytoskeleton components (microtubules and actin).

Related Experiment Videos

  • Studies on viral spread using cell culture models and potentially animal models.

    • Main Results:

    • VV utilizes host cell microtubules for efficient intracellular trafficking during entry and egress.
    • Actin polymerization beneath cell-surface virions propels virus particles for cell-to-cell dissemination.
    • Distinct VV particle morphologies are associated with different roles in viral spread.

    Conclusions:

    • Vaccinia virus employs sophisticated hijacking of host cell machinery for its lifecycle.
    • Microtubule-dependent transport and actin-based motility are key for VV's intracellular and intercellular spread.
    • The study highlights the complex interplay between VV and host cells, with implications for antiviral strategies.