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The role of sialic acid in human polyomavirus infections

Gretchen V Gee1, Aisling S Dugan, Natia Tsomaia

  • 1Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA.

Glycoconjugate Journal
|April 1, 2006
PubMed

Insights

Human polyomaviruses JC virus (JCV) and BK virus (BKV) infect most people. Viral entry for both JCV and BKV depends on sialic acid interactions, influencing disease tropism.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • JC virus (JCV) and BK virus (BKV) are common human polyomaviruses infecting ~85% of the global population.
  • JCV causes progressive multifocal leukoencephalopathy (PML), a fatal demyelinating brain disease.
  • BKV is associated with polyomavirus-associated nephropathy (PVN) in kidney transplant recipients.

Purpose of the Study:

  • To review the known biology of human polyomaviruses JCV and BKV.
  • To elucidate the critical role of sialic acid in viral entry and tropism for JCV and BKV.

Main Methods:

  • Literature review of recent advances in polyomavirus research.
  • Analysis of studies investigating viral-host interactions.
  • Focus on sialic acid's role in viral tropism.

Main Results:

  • JCV and BKV are widespread human pathogens with significant disease potential.
  • Viral entry mechanisms for both JCV and BKV are critically dependent on sialic acid.
  • Sialic acid interactions are key determinants of viral tropism.

Conclusions:

  • Understanding the basic biology of JCV and BKV is crucial due to their disease-causing potential.
  • Sialic acid is a pivotal factor in mediating the entry and tropism of human polyomaviruses.
  • Further research into sialic acid's role may reveal therapeutic targets.

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