|MAUGHAN, MICHELE - University Of Delaware|
|DOUGHERTY, LORNA - University Of Delaware|
|PRESKENIS, LAUREN - University Of Delaware|
|LADMAN, BRIAN - University Of Delaware|
|GELB, JACK - University Of Delaware|
|KEELER, CALVIN - University Of Delaware|
Submitted to: Virology Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/12/2013
Publication Date: 3/23/2013
Publication URL: http://handle.nal.usda.gov/10113/60144
Citation: Maughan, M., Dougherty, L., Preskenis, L., Ladman, B., Gelb, J., Spackman, E., Keeler, C. 2013. Transcriptional analysis of the innate immune response of ducks to different species-of-origin low pathogenic H7 avian influenza viruses. Virology Journal. 10:94. DOI: 10.1186/1743-422X-10-94.
Interpretive Summary: Avian influenza virus (AIV) rarely causes disease in its natural host species such as ducks. However it is not known why ducks are resistant to disease in contrast to chickens and turkeys. It is believed that the immune response of ducks differs from other avian species which leads to a non-clinical infection, but one where high levels of virus are still spread. In order to understand this, which is a step toward understanding the ecology, evolution and epidemiology of the virus, this study looked at the effects virus exposure on gene in ducks. Domestic ducks (Pekin ducks) which are closely related to mallard ducks were tested. Tissues from the immune systems of euthanized ducks exposed to AIV strains from ducks, chickens and turkeys were tested for gene expression. It was shown that hundreds of genes are affected by AIV exposure and that they can vary by virus isolate. The functions of several of these genes are known to be involved in the immune response. The data here provides information that viruses from ducks are not targeted by the immune system the same way as all viruses and it provide specific information on how the duck’s body interacts with the virus.
Technical Abstract: Background: Ducks represent an important reservoir for avian influenza (AI) viruses and are partly responsible for the worldwide dissemination of AI. Due to the ability of some low pathogenicity avian influenza viruses (LPAIV) of the hemagglutinin H7 subtype to mutate into a highly pathogenic form of the virus, the H7 AI viruses are of epidemiological and economic importance. Thus far, however, relatively little work has been conducted on elucidating the host-pathogen interactions of ducks and H7 LPAIVs. In the current study, three H7 LPAIVs isolated from either chicken, duck, or turkey avian species were evaluated for their comparative effect on the transcriptional innate immune response of ducks. Results: Three H7 LPAIV isolates, chicken-origin (A/chicken/Maryland/MinhMa/2004), duck-origin (A/pintail/Minnesota/423/1999), and turkey-origin (A/turkey/Virginia/SEP-67/2002) were used to infect Pekin ducks. At 3 days post-infection, RNA from spleen tissue was used for transcriptional analysis using the Avian Innate Immune Microarray and quantitative real-time RT-PCR. Microarray analysis revealed a core set of 61 genes differentially regulated in response to all three LPAIVs tested and 101, 135, and 628 differentially expressed genes unique to infection with the chicken-, duck-, or turkey-origin LPAIV isolates respectively. qRT-PCR results revealed significant up-regulation of IL-1ß, IL-2, and IFN', especially with the chicken-origin isolate. Several key innate immune pathways were activated in response to LPAIV infection including the toll-like receptor and RIG-I-like receptor pathways. Conclusions: Ducks elicit a unique innate immune response to different species-of-origin H7 LPAIV isolates, however, a subset of genes are differentially expressed regardless of isolate origin. This core set of genes expressed in response to H7 LPAIVs represent several innate immune pathways critical to the duck immune response to AI. These data provide insight into the potential mechanisms employed by ducks to tolerate AI viral infection while remaining subclinical.