Genomic and antigenic properties of Newcastle Disease virus genotypes
2.XX1 and 2.VII from Egypt do not point to antigenic drift as a driving
force of spread
Abstract
Newcastle disease (ND), caused by avian orthoavulavirus type-1 (NDV), is
endemic in poultry in the Middle East causing continuing outbreaks in
poultry populations despite efforts to vaccinate. In the past, genotype
2.XXI (former 2.VI) was present in poultry in Egypt but has been
replaced by genotype 2.VII. We investigated whether virus evolution
contributed to superseding, and focused on the antigenic sites within
the Heamagglutinin-Neuramindase (HN) spike protein. Full length
sequences of a NDV genotype 2.VII isolate currently circulating in Egypt
was compared to a genotype 2.XXI isolate that was present as
co-infection with vaccine type viruses (2.II) in an historical isolate
of the year 2011. Amino acid differences in the HN glycoprotein for both
2.XXI and 2.VII viruses amounted to 11,7% and 11,9 % compared to
LaSota vaccine type. However, mutations within the globular head (aa
126-570), bearing relevant antigenic sites, were underrepresented (aa
divergence of 8,8% and 8,1 % compared to 22,4% and 25,6% within the
fragment encompassing cytoplasmic tail, transmembrane part and stalk
regions (aa 1-125) for genotypes 2.XXI and 2.VII, respectively.
Nevertheless, reaction patterns of HN-specific monoclonal antibodies
revealed differences between vaccine type viruses and genotype 2.XXI and
2.VII viruses for specific epitopes. Accordingly, compared to Egyptian
vaccine type isolates and the LaSota vaccine reference strain, single aa
substitutions in 6 of 10 described neutralizing epitopes were found
within the attachment protein. However, the same alterations in
neutralization sensitive epitopes were present in old genotype 2.XXI as
well as in newly emerged genotype 2.VII isolates. In addition, isolates
were indistinguishable by polyclonal chicken sera raised against
different genotypes including vaccine viruses. These findings suggest,
that factors other than antigenic differences within the HN-protein
account for facilitating spread of genotype 2.VII while displacing
genotype 2.XXI viruses in Egypt.