This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gilbert, J. Articles by Benjamin, T. Search for Related Content PubMed PubMed Citation Articles by Gilbert, J. Articles by Benjamin, T.

 Previous Article  |  Next Article 

Journal of Virology, January 2005, p. 615-618, Vol. 79, No. 1
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.1.615-618.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Ganglioside GD1a Restores Infectibility to Mouse Cells Lacking Functional Receptors for Polyomavirus

Joanna Gilbert,¹ Jean Dahl,¹ Cathy Riney,¹ John You,¹ Cunqi Cui,^1, Randall Holmes,² Wayne Lencer,³ and Thomas Benjamin^1*

Department of Pathology,¹ G.I. Cell Biology, Children's Hospital, Harvard Medical School, Boston, Massachusetts,³ Department of Microbiology, University of Colorado Health Sciences Center, Denver, Colorado²

Received 17 June 2004/ Accepted 6 August 2004

Recent investigations on the pathway of cell entry by polyomavirus (Py) and simian virus 40 (SV40) have defined specific gangliosides as functional receptors mediating virus binding and transport from the plasma membrane to the endoplasmic reticulum (B. Tsai et al., EMBO J. 22:4346-4355, 2003; Gilbert and Benjamin, in press). These studies were carried out with C6 rat glioma cells, a heterologous host chosen for its known deficiency in ganglioside biosynthesis. Here, a cell genetic approach was undertaken to identify components required for the early steps of infection using mouse cells as the natural host for Py. Receptor-negative (R–) mouse cells, screened based on resistance to Py infection, were shown to bind Py but failed to allow entry of the virus. R– cells were also found to be resistant to SV40. Infectibility was restored or enhanced by the addition of the same specific gangliosides found in earlier studies with C6 cells. In one R– line, overexpression of caveolin-1 also increased infectibility. These results support and extend findings on gangliosides in lipid rafts as functional receptors and mediators of internalization for Py and SV40.

Present address: Department of Genetics, Rutgers University, Piscataway, NJ 08854.

This article has been cited by other articles:

• Desai, P. T., Walsh, M. K., Weimer, B. C. (2008). Solid-Phase Capture of Pathogenic Bacteria by Using Gangliosides and Detection with Real-Time PCR. Appl. Environ. Microbiol. 74: 2254-2258 [Abstract] [Full Text]  
• Dugan, A. S., Gasparovic, M. L., Atwood, W. J. (2008). Direct Correlation between Sialic Acid Binding and Infection of Cells by Two Human Polyomaviruses (JC Virus and BK Virus). J. Virol. 82: 2560-2564 [Abstract] [Full Text]  
• Schmidt, M., Chiorini, J. A. (2006). Gangliosides are essential for bovine adeno-associated virus entry.. J. Virol. 80: 5516-5522 [Abstract] [Full Text]  
• Liebl, D., Difato, F., Hornikova, L., Mannova, P., Stokrova, J., Forstova, J. (2006). Mouse Polyomavirus Enters Early Endosomes, Requires Their Acidic pH for Productive Infection, and Meets Transferrin Cargo in Rab11-Positive Endosomes. J. Virol. 80: 4610-4622 [Abstract] [Full Text]  
• Low, J. A., Magnuson, B., Tsai, B., Imperiale, M. J. (2006). Identification of Gangliosides GD1b and GT1b as Receptors for BK Virus. J. Virol. 80: 1361-1366 [Abstract] [Full Text]