The role of sialic acid in human polyomavirus infections.
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.
Gee
Gretchen V
GV
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA.
Dugan
Aisling S
AS
Tsomaia
Natia
N
Mierke
Dale F
DF
Atwood
Walter J
WJ
D006801:Humans; D019158:N-Acetylneuraminic Acid / Q000378:metabolism*; D011120:Polyomavirus / Q000472:pathogenicity* / Q000502:physiology*; D027601:Polyomavirus Infections / Q000821:virology*; D011991:Receptors, Virus / Q000737:chemistry / Q000378:metabolism
D011991:Receptors, Virus; D019158:N-Acetylneuraminic Acid