Newcastle disease (ND) is caused by virulent strain, responsible for serious economic losses to the poultry industry worldwide. Sporadic outbreaks in Pakistan necessitate the need of proper diagnosis and vaccination. Previous studies from various parts of Pakistan in commercial, backyard and wild birds indicated the involvement of multiple genotypes.
Molecular research has gained a lot of novel information about its causative agent by exploring its potential to induce disease in different avian species. However, genomic, immunological and patho-biological aspects of wild bird originated ND viruses have received little attention. This may be attributed to the lack of molecular facilities and epigenetic immune function. With this background, molecular studies focusing the genetic variation in ND viruses and expression of genetic profile following experimental challenge in commercial poultry has been investigated. The viruses were isolated from green winged teal and pigeons. The biologic and genomic evaluation based results proposed that pigeon isolates belonged to genotype VI and sub-genotype ‘m’ as mesogenic whereas teal/duck was found to have genotype VII and sub-genotype ‘i’ as velogenic. Interestingly, when compared with vaccine strain (LaSota), the results of present study showed differences in the antigenic epitopes of fusion and HN proteinsforcurrently circulating ND viruses.
Both strains showed their ability to transmit and infection to commercial poultry and pigeons. Furthermore, a comparison of gene profile of both strains has resulted insignificant difference in the number and level of expressed genes in infected lung and spleen samples. Current study highlights the significant differences in Host innate immune responses and pathogenesis in form of differentially expressed genes.
A total of 110 innate immune related genes were found to be differentially expressed in infected lung and spleen tissues. Inflammatory and cytokines associated genes were found to be down-regulated in spleen as compared to lung. While, toll like receptors and interferon stimulated genes were found to be up-regulated in both tissues infected with both strains.
Aziz-ul-Rahman
Lahore
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