Additional Glycosylation at the Receptor Binding Site of the Hemagglutinin (HA) for H5 and H7 Viruses May Be an Adaptation to Poultry Hosts, but Does It Influence Pathogenicity?
- 1 September 2003
- journal article
- Published by American Association of Avian Pathologists (AAAP) in Avian Diseases
- Vol. 47 (s3) , 942-950
- https://doi.org/10.1637/0005-2086-47.s3.942
Abstract
Sequence analysis of the hemagglutinin (HA) gene of H5 and H7 viruses was used to determine phylogenetic relationships between high-pathogenicity avian influenza (HPAI) and low-pathogenicity avian influenza (LPAI) viruses from avian influenza (AI) outbreaks in Norfolk in 1979 and 1991 and Italy in 1999–2000. A common feature within these groups of viruses was the acquisition of additional glycosylation sites near the receptor binding site of the HA. Passage of H5 viruses through 14-day-old embryonated fowls' eggs readily selected viruses with additional glycosylation of HA1. Although additional glycosylation may not correlate with increased pathogenicity for fowl, it may predispose viruses to become highly pathogenic. La glucosilación adicional del sitio de unión al receptor de la hemoaglutinina para los virus H5 y H7 puede ser una adaptación al huésped aviar, pero puede influencias la patogenicidad? Se emplearon análisis de las secuencias del gen hemoaglutinina (HA) de los virus H5 y H7 para determinar las relaciones filogenéticas entre los virus de influenza de patogenicidad alta y baja en los brotes de Norfolk en 1979 y en 1991 y de Italia en 1999 y el 2000. Una característica común dentro de estos grupos de virus fue la adquisición de sitios de glucosilación adicionales cerca del sitio de recepción en la hemoaglutinina. Los pasajes de los virus H5 en huevos embrionados de aves de 14 días de edad seleccionaron virus con sitios de glucosilación adicionales en la hemoaglutinina 1 (HA1). Aunque los sitios de glucosilación nuevos pueden no tener correlación con el incremento en la patogenicidad para las aves domésticas, si pueden predisponer a los virus para que sean más patógenos. Abbreviations: AI = avian influenza, CPE = cytopathic effect, HA = hemagglutinin, HPAI = high-pathogenicity avian influenza, ICPI = intracerebral pathogenicity indices, IVPI = intravenous pathogenicity indices, LPAI = low-pathogenicity avian influenza, MDCK = Madin–Darby canine kidneyKeywords
This publication has 9 references indexed in Scilit:
- Changes in the haemagglutinin and the neuraminidase genes prior to the emergence of highly pathogenic H7N1 avian influenza viruses in ItalyArchiv für die gesamte Virusforschung, 2001
- Interdependence of Hemagglutinin Glycosylation and Neuraminidase as Regulators of Influenza Virus Growth: a Study by Reverse GeneticsJournal of Virology, 2000
- Structural features of the avian influenza virus hemagglutinin that influence virulenceVeterinary Microbiology, 2000
- Phylogenetic analysis of H7 haemagglutinin subtype influenza A virusesArchiv für die gesamte Virusforschung, 2000
- Characterisation of an avian influenza A virus isolated from a human – is an intermediate host necessary for the emergence of pandemic influenza viruses?Archiv für die gesamte Virusforschung, 1998
- Do Hemagglutinin Genes of Highly Pathogenic Avian influenza Viruses Constitute Unique Phylogenetic Lineages?Virology, 1995
- Deduced amino acid sequences of the haemagglutinin of H5N1 avian influenza virus isolates from an outbreak in turkeys in Norfolk, EnglandArchiv für die gesamte Virusforschung, 1994
- An outbreak of highly pathogenic avian influenza in turkeys in Great Britain in 1991Published by Wiley ,1993
- Evolutionary trees from DNA sequences: A maximum likelihood approachJournal of Molecular Evolution, 1981