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 In the past, genotype 2.XXI (former 2.VI) was present in poultry in Egypt but has been replaced by genotype 2.VII.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.