Genetic mechanisms involved in the evolution of the terminal overlapping VP5 gene of the Infectious Bursal Disease Virus.

HERNANDEZ, MARTIN; MAYA, LETICIA; TOMAS, GONZALO; BIALADE, FEDERICA; BENITEZ, MARIA JOSE; PANZERA, YANINA; HERNANDEZ, DIEGO; AGUIRRE, SEBASTIAN; MATTION, NORA; PEREZ, RUBEN

Punta del Este, Uruguay

Congreso; Darwin 200 South American celebration; 2009

Darwin 200 South American celebration

Since its discovery in 1962, the Infectious Bursal Disease Virus (IBDV) (Birnaviridae family) has represented one of the main threatens to the poultry industry worldwide. The molecular characterization of different IBDV genomic regions has been essential for the epidemiological understanding of this viral model. However most of the mechanisms that have shaped the evolution of IBDV are still unknown. Here, we accomplished an evolutionary study of the gene that codifies the non-structural VP5 protein. The VP5 gene, which has lately acquired relevance because it seems to be related to the viral pathogenicity, terminally overlaps with the coding region of the major structural protein VP2. By a detailed comparative analysis of about fifteen VP5 sequences belonging to the three existent IBDV strains (classic (c), variant (va), and very virulent (vv)), including VP5 sequences of South American field isolates characterized for the first time in this study, we found that the evolution of the VP5 gene is highly influenced by the evolution of the VP2 one. Selective pressures analysis using the dN/dS ratio revealed the existence of a strong purified selection exerted on the 5’ terminal overlapping extreme of VP2 that indirectly constrains the evolution of VP5. These results reinforce the hypothesis that the non-structural protein VP5 gene was originated lately in the IBDV evolution by a mechanism of genetic overprinting. We also found VP5 genes in vvIBDV field isolates that lack the alternative AUG start codon, characteristic of the hypervirulent strains described until now. Consequently, these vvIBDV would have a 145 amino acid long VP5 protein rather than the putative 149 amino acid long protein of the hypervirulent strains. This finding is an evidence that the VP5 could be not only differentially evolving by the acquisition of point mutations along the gene but also by a potential variation of the translation initiation site.   Since the VP5 seems to be related with viral pathogenicity, information provided by this kind of evolutionary studies should be useful to highlight the impact of the genetic variation in this non-structural protein on the epidemiology of IBDV.