Lipids and proteins act in opposing manners to regulate polyomavirus infection.

Abstract

How receptors control virus infection is poorly understood. Polyomavirus (Py) binds to the sialic acid-galactose moiety on receptors to gain entry into host cells and cause infection. We previously demonstrated that the sialic acid-galactose-containing glycolipids called gangliosides GD1a and GT1b promote Py infection, in part, by sorting the virus from the endolysosomes to the endoplasmic reticulum (ER), a critical infection route. Whether these glycolipids act as Py entry receptors, however, is not clear. Additionally, as the majority of glycoproteins also harbor terminal sialic acid-galactose residues, their roles in Py infection are also not well established. Using a ganglioside-deficient cell line, we show that GD1a is the functional entry receptor for Py. GD1a binds to Py on the plasma membrane, and the receptor-virus complex is internalized and transported to the late endosomes and then the ER to initiate infection. In contrast, our findings indicate that glycoproteins act as decoy receptors, restricting the ER transport and infection of Py. Thus, glycolipids and glycoproteins, two major constituents of the plasma membrane, execute opposing functions in regulating infection by a defined virus.

• Authors: Mengding Qian, Billy Tsai
• Journal: Journal of virology (J Virol) Vol. 84 Issue 19 Pg. 9840-52 (Oct 2010) ISSN: 1098-5514 [Electronic] United States
• PMID: 20668088 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene
• Boron Compounds
• Fluorescent Dyes
• Gangliosides
• Membrane Lipids
• Membrane Proteins
• Receptors, Virus
• ganglioside, GD1a
• trisialoganglioside GT1

Topics

• Animals
• Biological Transport, Active
• Boron Compounds
• Cell Line
• Endoplasmic Reticulum (metabolism, virology)
• Endosomes (metabolism, virology)
• Fluorescent Dyes
• Gangliosides (metabolism)
• Membrane Lipids (metabolism)
• Membrane Proteins (metabolism)
• Mice
• Models, Biological
• NIH 3T3 Cells
• Polyomavirus (pathogenicity, physiology)
• Polyomavirus Infections (metabolism, virology)
• Receptors, Virus (metabolism)
• Virus Internalization