Location: Location not imported yet.Title: Immediate early responses of avian tracheal epithelial cells to infection with highly pathogenic avian invluenza virus) Author
Submitted to: Biologicals
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/20/2007
Publication Date: 3/20/2008
Citation: Sarmento, L., Pantin Jackwood, M.J., Kapczynski, D.R., Swayne, D.E., Afonso, C.L. 2008. Immediate early responses of avian tracheal epithelial cells to infection with highly pathogenic avian invluenza virus. Biologicals. 132:175-183. Interpretive Summary: Avian influenza is a major viral disease of poultry that occurs worldwide and leads to significant financial losses. Losses are caused by the death of the birds infected with the virus, culling of infected and likely infected birds to control the spread of the virus, and from restrictions on export of poultry and poultry products from the region of the outbreak. Currently live attenuated vaccines are not used because of significant concerns over stability and safety. In order to improve our ability to protect naïve birds from infection and to create live attenuated vaccines basic knowledge on the early host responses and the mechanism of innate immunity are needed. Here we describe the establishment of chicken and duck tracheal epithelial cell culture system and the study of early responses to infection using microarrays as new tools to identify molecular changes that occur at mucosal sites of early AIV infection.
Technical Abstract: Highly pathogenic (HP) avian influenza viruses (AIV) present an ongoing threat to the world poultry industry. In order to develop new AIV control strategies it is necessary to understand the underlying mechanism of viral infection at mucosal respiratory sites. Chicken and duck tracheal epithelial cells systems (TEC) were developed to study early host responses to AIV infection on TEC. Infection of 2 week-chickens and ducks with the highly pathogenic AIV H5N1 Ck/Hong Kong/220/97 and Egret/Hong Kong/757.2/02 viruses together with TEC early responses to infection suggest the induction of differential innate immune responses. Growth curves indicated that although chicken and ducks TEC supported viral replication and re-infection, the capacity of the two viruses to replicate was not equal. A 42K gene chicken microarray system used to characterize differences in gene expression between chicken tracheal epithelial cells infected with these two highly pathogenic AIV identified expression of virus-specific molecular markers. The existence of dissimilar patterns of host gene expression as early as six hours post infection suggest that the differential growth characteristics of the two highly pathogenic AIV in tracheal epithelial cells is preceded by distinct host responses.