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Title:   Author  item
                                            Pantin Jackwood, Maryitem
                                            Lee, Changitem
                                            Kapczynski, Darrellitem
                                            Sarmento, Lucianaitem
                                            Wasilenko, Jamieitem
                                            Spackman, Ericaitem
                                            Suarez, David
  Submitted to: Options for the Control of Influenza Conference
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 5/1/2007
                                    Publication  Date: 6/17/2007
                                    Citation: Pantin Jackwood, M.J., Lee, C.W., Kapczynski, D.R., Sarmento, L., Wasilenko, J.L., Spackman, E., Suarez, D.L. 2007. Pathogenesis of H5N1 avian influenza virus gene reassortants in chickens [abstract]. Options for the Control of Influenza VI Conference, Abstract book. June 17-23, 2007, Toronto, Canada. p. 260.Interpretive Summary:
                                Technical Abstract: Highly pathogenic H5N1 avian influenza viruses produce severe disease and mortality in chickens.  Identification of viral genes important for cell tropism and replication efficiency helps identify and target virulence factors.  To determine which viral gene or genes contribute to the virulence of H5N1 avian influenza viruses in chickens, we used reverse genetics to generate single-gene recombinant viruses and examined their pathogenicity in chickens.  Intranasal inoculation of two week-old chickens with the recombinant avian influenza virus rEgret/HK/02 resulted in 100% mortality and high viral titers in tissues.  Inoculation of chickens with rCk/Indonesia/03 produced only 50% mortality with significantly less viral replication in tissues.  Reassortants combining genes of the mentioned viruses demonstrated that exchanging the hemagglutinin and PB2 genes considerably affected pathogenicity; this was reflected in increased mortality and increased viral replication and spread in tissues.  The NS gene also had an effect on viral replication; however, no effect on mortality was observed.  Differences in interferon-alpha (IFNalpha) mRNA cytokine levels in lung and spleen correlated with differences observed in pathogenicity among the recombinant viruses.


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