Sequence and Phylogenetic Analysis of P10- and P17-Encoding Genes of Avian Reovirus
Avian reovirus (ARV) causes viral arthritis, chronic respiratory diseases, and malabsorption syndrome. The P10 protein is a viroporin and induces cell fusion, whereas the biological function of P17 protein is completely unknown. In this study, the nucleotide sequences of the P10- and P17-encoding ge...
Gespeichert in:
Veröffentlicht in: | Avian diseases 2005-03, Vol.49 (1), p.36-42 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Avian reovirus (ARV) causes viral arthritis, chronic respiratory diseases, and malabsorption syndrome. The P10 protein is a viroporin and induces cell fusion, whereas the biological function of P17 protein is completely unknown. In this study, the nucleotide sequences of the P10- and P17-encoding genes from 17 field isolates and vaccine strains of ARV isolated over a 23-year period from distinct geographic locations were analyzed to define phylogenetic profiles and to study sequence variability and genetic evolution. These genes displayed the signs of a high level of sequence divergence and have evolved into five distinct lineages, respectively. The P17-encoding gene showed higher sequence divergence than that of P10-encoding gene. Our results indicated that synonymous substitutions predominate over nonsynonymous substitutions in both genes. Comparison of P10 and P17 gene phylograms with those of S-class genes revealed distinct evolutionary patterns, indicating that P10 and P17 evolve in an independent manner. Comparative sequence analysis also showed extensive sequence divergence between ARV and other orthoreoviruses. The phylogenetic analysis of P10- and P17-encoding genes revealed that diversity within both genes is neither dependent of viral serotypes nor correlated with the disease states caused by avian reovirus. |
---|---|
ISSN: | 0005-2086 1938-4351 |
DOI: | 10.1637/7264-081904R1 |