بررسی مولکولی ژن هماگلوتنین- نورآمینیداز فرم عصبی ویروس بیماری نیوکاسل جدا شده از شمال ایران

During recent decades, there have been numerous reports of Newcastle virus infection and isolation in industrial poultry, rural, and wild birds. The presence of a highly contagious and lethal disease implies the occurrence of genetic mutations in the virus, which could potentially due to the breakdown of the immune barrier from vaccination in certain instances. The hemagglutinin-neuraminidase protein plays a crucial role in the process of immune induction. Alignment analysis revealed a reduction in similarity at both the nucleotide and amino acid levels when comparing the isolates examined in this study with the vaccine strains. Moreover, the analysis of alterations in the neutralizing epitope pattern exhibited substitutions at the amino acid level in positions 347 (E to Q), 356 (R to K), 363 (N to K), 494 (G to D), and 514 (I to V) as compared to the vaccine strains. These results, proposed that these mutations may contribute to the antigenic modifications in novel strains of the virus. The glycosylation profile modifications were found to be associated with excision and introduction at positions 538 and 144, respectively, as opposed to the vaccinal strains.Therefore, it is essential to design and carry out further research studies to determine the impact of these mutations and glycosylation patterns on the virulence and ability of new viral strains to promote pathogenicity and escape immunization derived from vaccinal strains and develop potent new vaccines that specifically target these strains.