Author
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Swayne, David |
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Submitted to: Meeting Abstract
Publication Type: Abstract Only Publication Acceptance Date: 4/1/2006 Publication Date: 6/29/2006 Citation: Swayne, D.E. 2006. Widening host range and changing pathobiology of Eurasian H5N1 avian influenza in domestic and wild birds [abstract]. In: Proceedings of the First International Conference on Avian Influenza in Humans. p. 17. Interpretive Summary: Technical Abstract: Avian influenza (AI) viruses are classified into 16 different hemagglutinin and 9 different neuraminidase subtypes, and two phenotypes, high (HP) and low pathogenicity (LP), based on virulence for chickens. However, other criteria are important in understanding the complex pathobiology of AI viruses including host exposure and virus adaptation, transmissibility, infectivity, and pathogenicity. Overall, such pathobiological features vary with host species and virus strain. LPAI viruses infect epithelial cells of respiratory and intestinal tracts, producing limited localized infections in various bird species. By contrast, HPAI viruses typically produce a severe, systemic disease with high mortality in chickens and other galliforme birds. However, these same viruses usually produce no infection or only mild disease in domestic ducks and wild birds. Over the past decade, the emergent Asian H5N1 HPAI viruses have shifted to increased virulence for chickens as evident by shorter mean death times (MDT) and a greater propensity for massive replicate in vascular endothelial cells. Especially important, the Asia H5N1 HPAI viruses have changed from producing inconsistent respiratory infections in 2 week-old domestic ducks to some strains being highly lethal with virus being localized to internal organs and brain. However, the high lethality for ducks is inversely related to age verses in galliforme birds were HPAI virus are highly lethal irrespective of age. The most recent Asian H5N1 HPAI viruses have infected some wild birds producing systemic infections and death. Across all bird species, the ability to produce severe disease and death is associated with high virus replication titers in the host, especially in specific tissues such as brain and heart. |
