<p>The infectious bronchitis virus (IBV) causes significant losses in commercial poultry egg and meat production. Since its first emergence, the genotype GI-23 (Variant 2) has progressively increased its geographical distribution, shown a significant virulence, and challenged the vaccine efficacy. Global viral transmission could be attributed to multiple factors including human related activities such as poultry and vaccine trades while other contributing factors such as the role of wild birds cannot be neglected. Therefore, A total 260 full S1 GI-23 sequences were obtained from Genebank, structured and intensively analyzed. The recombination analyses were conducted using RDP5 and GARD on the total dataset to identify the possible recombinant events. The recombinant-free dataset (214 sequences) was phylogeographically analyzed using BEAST 1.10, then selection pressure analyses to identify the possible migration routes and selection pressure markers, respectively. Recombination analyses showed multiple internal recombination events in 17.6% of the sequences. Phylogeographic analysis suggested Central and Eastern European (CEE) countries (i.e., particularly Poland and Romania) as likely sources of American GI-23-like virus outbreaks. Interestingly, the selection pressure analyses indicated positive selection signals, identifying five codons in some previously distinguished critical positions such as 61, 94, 119, 127, and 197. The virus extended geographical spread as well as molecular evolution through recombination and positive selection in the spike gene poses a major concern for increased adaptation and enhanced pathogenicity in susceptible domesticated and probably wild birds. Further studies on the impact of both recombination events and the identified positive selection codons are highly recommended to elucidate the molecular evolution mechanisms of IBV GI-23.</p>

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Global transmission pathways and adaptive molecular evolution of avian infectious bronchitis GI-23 (Variant 2)

  • Mohamed H. Houta,
  • Giovanni Franzo,
  • Azza A. El-Sawah,
  • Matteo Legnardi,
  • Kareem E. Hassan,
  • Ahmed Ali,
  • Claudia M. Tucciarone,
  • Magdy F. Elkady,
  • Mattia Cecchinato,
  • Salama A. S. Shany

摘要

The infectious bronchitis virus (IBV) causes significant losses in commercial poultry egg and meat production. Since its first emergence, the genotype GI-23 (Variant 2) has progressively increased its geographical distribution, shown a significant virulence, and challenged the vaccine efficacy. Global viral transmission could be attributed to multiple factors including human related activities such as poultry and vaccine trades while other contributing factors such as the role of wild birds cannot be neglected. Therefore, A total 260 full S1 GI-23 sequences were obtained from Genebank, structured and intensively analyzed. The recombination analyses were conducted using RDP5 and GARD on the total dataset to identify the possible recombinant events. The recombinant-free dataset (214 sequences) was phylogeographically analyzed using BEAST 1.10, then selection pressure analyses to identify the possible migration routes and selection pressure markers, respectively. Recombination analyses showed multiple internal recombination events in 17.6% of the sequences. Phylogeographic analysis suggested Central and Eastern European (CEE) countries (i.e., particularly Poland and Romania) as likely sources of American GI-23-like virus outbreaks. Interestingly, the selection pressure analyses indicated positive selection signals, identifying five codons in some previously distinguished critical positions such as 61, 94, 119, 127, and 197. The virus extended geographical spread as well as molecular evolution through recombination and positive selection in the spike gene poses a major concern for increased adaptation and enhanced pathogenicity in susceptible domesticated and probably wild birds. Further studies on the impact of both recombination events and the identified positive selection codons are highly recommended to elucidate the molecular evolution mechanisms of IBV GI-23.