Glycoconjugate Journal

, Volume 23, Issue 1, pp 19–26

The role of sialic acid in human polyomavirus infections

  • Gretchen V. Gee
  • Aisling S. Dugan
  • Natia Tsomaia
  • Dale F. Mierke
  • Walter J. Atwood
Mini Review

DOI: 10.1007/s10719-006-5434-z

Cite this article as:
Gee, G.V., Dugan, A.S., Tsomaia, N. et al. Glycoconj J (2006) 23: 19. doi:10.1007/s10719-006-5434-z

Abstract

JC virus (JCV) and BK virus (BKV) are human polyomaviruses that infect approximately 85% of the population worldwide [1,2]. JCV is the underlying cause of the fatal demyelinating disease, progressive multifocal leukoencephalopathy (PML), a condition resulting from JCV induced lytic destruction of myelin producing oligodendrocytes in the brain [3]. BKV infection of kidneys in renal transplant recipients results in a gradual loss of graft function known as polyomavirus associated nephropathy (PVN) [4]. Following the identification of these viruses as the etiological agents of disease, there has been greater interest in understanding the basic biology of these human pathogens [5,6]. Recent advances in the field have shown that viral entry of both JCV and BKV is dependent on the ability to interact with sialic acid. This review focuses on what is known about the human polyomaviruses and the role that sialic acid plays in determining viral tropism.

Keywords

JCV BKV Sialic acid Polyomavirus 

Copyright information

© Springer Science + Business Media, LLC 2006

Authors and Affiliations

  • Gretchen V. Gee
    • 1
  • Aisling S. Dugan
    • 2
  • Natia Tsomaia
    • 3
  • Dale F. Mierke
    • 3
  • Walter J. Atwood
    • 4
  1. 1.Department of Molecular Biology, Cell Biology and BiochemistryBrown UniversityProvidence
  2. 2.Graduate Program in PathobiologyBrown UniversityProvidence
  3. 3.Department of Molecular Pharmacology, Physiology and BiotechnologyBrown UniversityProvidence
  4. 4.Department of Molecular Biology, Cell Biology and Biochemistry and Graduate Program in PathobiologyBrown UniversityProvidence