Submitted to: American Society for Virology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 4/4/2007
Publication Date: 7/24/2007
Citation: Yu, Q., Estevez, C., King, D.J., Miller, P.J. 2007. A Newcastle disease virus hemagglutinin-neuraminidase mutation that diminished hemagglutination and neuraminidase activity did not change infectivity and pathogenecity [abstract]. In: Proceedings of the 26th Annual Meeting of American Society for Virology, July 14-18, 2007, Corvallis, Oregon. p. 106.
Technical Abstract: Infection by Newcastle disease virus (NDV), a member of the Paramyxoviridae family, requires recognition and attachment of the virions to host cell receptors containing sialic acid residues. Recognition of sialic acid-containing proteins is mediated by the hemagglutinin-neuraminidase (HN) protein of the virus. Two active sites have been recognized on the globular head of the HN protein. Site one is thought to mediate the initial sialic acid receptor recognition and the neuraminidase activity of the protein, while site two, upon initial attachment of sialic acid to site one, also recognizes sialic acid-containing proteins on the host cell surface, stabilizing the attachment of the virion particle to the host cell. The hemagglutination (HA) activity of a NDV strain is generally considered as an indication of that virus attachment property. In this study, using reverse genetics, we have generated a NDV mutant with a single amino acid substitution in the HN protein at the position (I192M) near to the pocket that has been demonstrated to be part of the site one of the protein. This HN mutant has a highly diminished HA activity with chicken and turkey red blood cells in a microplate assay and has no detectable neuraminidase (NA) activity with the Amplex® Red neuraminidase assay. The absence of HA and NA activities indicates that site one is probably not able to recognize and attach to sialic acid in the host cells. To assess the effect of the mutation on virus activity in vivo we performed the mean death time (MDT) test, intracerebral pathogenicity index (ICPI) test, and intraocular inoculation of day old specific pathogen-free birds. There was no difference in the capability of the mutant virus to infect and cause disease in chickens and embryos, as compared to the rescued parental virus. The results demonstrate that the mutation near the HN site one that diminished HA activity and eliminated NA activity did not change the infectivity or pathogenicity of the virus.