Clinical Coxsackievirus B Isolates Differ from Laboratory Strains in Their Interaction with Two Cell Surface Receptors

• Published in: The Journal of infectious diseases Vol. 175; no. 3; pp. 697 - 700
• Main Authors: Bergelson, Jeffrey M., Modlin, John F., Wieland-Alter, Wendy, Cunningham, Jennifer A., Crowell, Richard L., Finberg, Robert W.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.03.1997; University of Chicago Press; Oxford University Press
• Subjects: Antibodies; Antibodies, Monoclonal; Antibodies, Viral - immunology; Bacteriology; Biogenesis of cell structures, supramolecular organization; Biological and medical sciences; CD55 Antigens - metabolism; Concise Communications; Coxsackievirus Infections - microbiology; Enterovirus; Enterovirus B, Human - metabolism; Enterovirus B, Human - pathogenicity; Fundamental and applied biological sciences. Psychology; HeLa Cells; Humans; Infections; Microbiology; Molecular interactions; Molecules; Monoclonal antibodies; Receptors; Receptors, Virus - metabolism; Transfection; Viruses; Picornaviridae; Coxsackievirus B; Receiver; Enterovirus; Experimental study; In vitro; Cell surface; Bacteriology; Virus; Phenotype; Relation; Immunology; Biological effect
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/175.3.697

Coxsackie B viruses interact with two putative cell surface receptor molecules. Experiments with prototype laboratory strains suggest that all 6 coxsackie B serotypes interact with a 46-kDa protein recognizedby the monoclonalantibody RmcB, whereas CB1, CB3, and CBSmay also bind to decay accelerating factor. Antireceptor monoclonal antibodies were used to study interactions between low-passage clinical coxsackie B virus isolates and the two receptors. In contrast to observations made with single prototype strains, these data indicate that receptor use by clinical isolates is not strictly related to serotype and that even prototype strains with different passage histories may differ in receptor use. Within a given serotype, variation exists in the capacity of individual virus isolates to bind to specific receptors, and variants with altered receptor specificity may arise during infection in humans and in tissue culture.