A synthetic sialic acid analog that is resistant to the receptor-destroying enzyme can be used by influenza C virus as a receptor determinant for infection of cells

A synthetic sialic acid analog, N-acetyl-9-acetamido-9-deoxy-neuraminic acid, can be used by influenza C virus as a receptor determinant for attachment to cells, In contrast to the natural determinant, N-acetyl-9-O-acetylneuraminic acid, the synthetic sialic acid is resistant to the action of the re...

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Hauptverfasser: Herrler, Georg (VerfasserIn) , Groß, Hans Jürgen (VerfasserIn) , Brossmer, Reinhard (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: November 22, 1995
In: Biochemical and biophysical research communications
Year: 1995, Jahrgang: 216, Heft: 3, Pages: 821-827
ISSN:1090-2104
DOI:10.1006/bbrc.1995.2695
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1006/bbrc.1995.2695
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0006291X85726952
Volltext
Verfasserangaben:Georg Herrler, Hans-Jürgen Gross, and Reinhard Brossmer
Beschreibung
Zusammenfassung:A synthetic sialic acid analog, N-acetyl-9-acetamido-9-deoxy-neuraminic acid, can be used by influenza C virus as a receptor determinant for attachment to cells, In contrast to the natural determinant, N-acetyl-9-O-acetylneuraminic acid, the synthetic sialic acid is resistant to the action of the receptor-destroying acetylesterase of this virus. The sialic acid analog was enzymatically transferred to the surface of Madin-Darby canine kidney cells that are resistant to infection because of a lack of receptors. Influenza C virus was able to infect the modified cells though requiring a 10-fold larger amount of the sialic acid analogue on the cell surface compared to the natural receptor determinant. The quantitative difference is accounted for mainly by a less efficient binding of influenza C virus to the analog. Thus, in our system, inactivation of the receptor by the viral esterase is not required for the initiation of an influenza C virus infection.
Beschreibung:Elektronische Reproduktion der Druck-Ausgabe 25. Mai 2002
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Beschreibung:Online Resource
ISSN:1090-2104
DOI:10.1006/bbrc.1995.2695