Glycosylation within an antigenic site on the HN glycoprotein of Newcastle disease virus interferes with its role in the promotion of membrane fusion

Virology
R DengRonald M Iorio

Abstract

The binding of monoclonal antibodies to antigenic site 3 on the hemagglutinin-neuraminidase (HN) glycoprotein of Newcastle disease virus neutralizes viral infectivity and prevents syncytium formation by a mechanism other than the prevention of viral attachment. The virus can escape neutralization by these antibodies by the addition of an N-glycan at a site introduced by a D287N mutation in HN. The variant has significantly reduced ability to induce fusion from within, the mode of fusion promoted by the viral glycoproteins deposited on the cell surface late in infection. Conversely, and unlike the parent virus, the variant has acquired the ability to promote fusion from without, the mode of fusion directly mediated by input virions at high multiplicity. This finding is consistent with different roles for the HN protein in virion-cell and cell-cell fusion. D287N-mutated HN with its additional N-glycan shows a markedly reduced ability, compared to wild-type HN, to complement the viral fusion protein in the promotion of fusion in a BHK cell transient expression system. This confirms that the addition of an N-glycan in HN antigenic site 3 and the deficiency in syncytium formation are causally related. Moreover, no alteration in cell...Continue Reading

Citations

Jun 15, 2010·Avian Pathology : Journal of the W.V.P.A·Guan M KeHung J Liu
May 2, 2003·Bioscience, Biotechnology, and Biochemistry·Hiroaki SegawaHideharu Taira
Jun 8, 2018·Glycobiology·Victoria OrtegaHector C Aguilar
Jul 3, 2021·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Irene MaierGeorg Kontaxis

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