|Pantin Jackwood, Mary
|LEE, CHANG WON - OARDC, OHIO STATE UNIV
Submitted to: International Poultry Forum Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 10/29/2007
Publication Date: 1/21/2008
Citation: Wasilenko, J.L., Pantin Jackwood, M.J., Sarmento, L., Lee, C., Suarez, D.L. 2008. Role of different genes in the pathogenesis of H5N1 avian influenza virus in chickens [abstract]. International Poultry Scientific Forum, January 21-22, 2008, Atlanta, Georgia. p. 24.
Technical Abstract: The determinants of pathogenicity of Avian Influenza (AI) virus are not totally defined. Previous studies have pointed towards the importance of different influenza virus genes in determining virulence in various hosts. We used reverse genetics to generate recombinant viruses in order to better understand the role of recombination in AI pathogenesis and to determine which viral genes contribute to the virulence of AI viruses in chickens. A recombinant virus, Ck/Indonesia/03, displayed 50-75% mortality in chickens. Single genes in this virus were then replaced with those from a rEgret/HK/02 virus which displays 100% mortality and high viral titers in tissues. Pathogenicity of the viruses in chickens was then studied. Exchange of the HA gene considerably affected virulence which was reflected in increased mortality, increased viral replication and spread in tissues, demonstrating the importance of the HA gene in pathogenesis of the virus. The HA genes had identical cleavage sites however there were 11 amino acid differences, 5 located in the receptor binding site of the glycoprotein, which could explain the difference observed in pathogenicity of the viruses. Exchange of the NS, NP or M genes also resulted in decreased mean death times (MDT), increased viral replication and spread of the virus in tissues compared to the rIndonesia/HK/02 parent virus. Replacing the NP gene resulted in a virus with the shortest MDT and increased viral spread in tissues, surpassing that of the HA gene recombinant. Exchanging either the PB2 or PB1 genes did not result in increased virulence suggesting these polymerase genes may function more effectively as a unit derived from the same viral strain.