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Related Experiment Videos

Parvovirus host range, cell tropism and evolution.

Karsten Hueffer1, Colin R Parrish

  • 1JA Baker Institute for Animal Health, Department of Microbiology Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.

Current Opinion in Microbiology
|August 28, 2003
PubMed
Summary
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Parvovirus evolution is driven by capsid structure, with transferrin receptor (TfR) binding enabling canine parvovirus emergence. Capsid spikes influence host range and tropism, shaping viral evolution.

Area of Science:

  • Virology
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Recent advances have significantly improved understanding of parvovirus evolution, host range, and cell tropism.
  • Key findings include the identification of transferrin receptor (TfR) as the cell surface receptor for canine parvovirus and feline panleukopenia virus.
  • The emergence of canine parvovirus as a novel pathogen in dogs was linked to specific binding to the canine TfR.

Purpose of the Study:

  • To elucidate the structural and functional basis of parvovirus host range and tropism.
  • To understand the evolutionary pressures shaping parvovirus adaptation.
  • To investigate the role of capsid structure in parvovirus-host interactions.

Main Methods:

  • Structural analysis of parvovirus capsids (e.g., adeno-associated virus-2, porcine parvovirus, minute virus of mice).

Related Experiment Videos

  • Structure-function studies to assess the role of capsid components, particularly threefold spikes.
  • Investigation of receptor binding interactions, including canine parvovirus and TfR.

    • Main Results:

    • The transferrin receptor (TfR) was identified as the cell surface receptor for canine parvovirus and feline panleukopenia virus.
    • Specific binding to the canine TfR facilitated the emergence of canine parvovirus in dogs.
    • Capsid structure, particularly threefold spikes, was shown to control cell tropism and host range in various parvoviruses.
    • Adeno-associated virus serotype tropisms were partly attributed to specific receptor binding.

    Conclusions:

    • Capsid structure, especially threefold spikes, plays a critical role in determining parvovirus cell tropism and host range.
    • Selective pressures acting on capsid-receptor interactions drive parvovirus evolution and adaptation.
    • Understanding these mechanisms is crucial for comprehending parvovirus emergence and pathogenesis.