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Journal of Virology, April 2002, p. 4087-4095, Vol. 76, No. 8
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.8.4087-4095.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Initial Interaction of Rotavirus Strains with N-Acetylneuraminic (Sialic) Acid Residues on the Cell Surface Correlates with VP4 Genotype, Not Species of Origin
Max Ciarlet,1* Juan E. Ludert,2 Miren Iturriza-Gómara,3 Ferdinando Liprandi,2 James J. Gray,3 Ulrich Desselberger,3 and Mary K. Estes1
Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030,1
Centro de Microbiología y Biología Celular, Instituto Venezolano de Investigaciones Científicas, Caracas 1020-A, Venezuela,2
Clinical Microbiology and Public Health Laboratory, Addenbrooke's Hospital, Cambridge CB2 2QW, United Kingdom3
Received 24 August 2001/
Accepted 10 December 2001
We examined 41 human and animal rotavirus strains representative of all known P genotypes for their dependency on cellular N-acetylneuraminic (sialic) acid (SA) residues for infectivity. Our results showed that all rotaviruses studied, whether of animal or human origin, belonging to P genotypes [1], [2], [3], and [7] depended on SA residues on the cell surface for efficient infectivity but that all human and animal rotavirus strains representative of the remaining known P genotypes were SA independent. The SA residue requirement for efficient infectivity did not change for reassortant rotavirus strains with altered VP4-VP7 combinations. The initial interaction of rotavirus strains with SA residues on the cell surface correlated with VP4 genotype specifity, not with species of origin or VP7 G serotype specificity (P = 0.001; r2 = 1.00, Pearson's correlation coefficient). In addition to being a requirement for infectivity, the presence of SA residues on the cell surface is a requirement for efficient growth in cell culture; recognition of the association of specific P genotypes with the binding of rotavirus to SA residues will facilitate our understanding of the molecular basis of the early events of rotavirus-cell interactions in cell culture models and of pathogenicity in vivo.
* Corresponding author. Mailing address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Room 921E, Mailstop BCM-385, Houston, TX 77030. Phone: (713) 798-4445. Fax: (713) 798-3586. E-mail:
mciarlet{at}bcm.tmc.edu.
Journal of Virology, April 2002, p. 4087-4095, Vol. 76, No. 8
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.8.4087-4095.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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