Meeting Abstract
P1.39 Tuesday, Jan. 4 Comparative Avian Immunogenetics: An Exploration of Antiviral Genes in Several Wild Bird Species ALTRICHTER, A. M.*; FASSBINDER-ORTH, C.A.; Creighton University; Creighton University cfa54967@creighton.edu
Many wild bird species are reservoirs for various arboviruses including West Nile virus and Western equine encephalitis virus. However, little is known about avian arbovirus infections or host antiviral immune responses. The goal of this project was to establish a technique to measure the immune response of wild birds to arbovirus infections. We chose Buggy Creek Virus (BCRV) as our model avian arbovirus system. BCRV is part of the western equine encephalomyelitis antigenic complex of arboviruses, and is transmitted by the swallow bug to the cliff swallow (Petrochelidon pyrrhonota). House sparrows (Passer domesticus) have usurped cliff swallow nests and thus, are exposed to the virus. We chose these two species along with zebra finch, (Taeniopygia guttata) to use as an evolutionary baseline. We used polymerase chain reaction (PCR) and reverse transcription polymerase chain reaction (RT-PCR) to determine the homologies among the selected bird species for six pattern recognition receptors (PRRs) including RIG-1, MDA5, Toll-like receptors 2,3,4, and 7, and six cytokines: Interferon-α, Interferon-γ, Interleukin 1β,4, 6, and 10. The two housekeeping genes we chose to study were β-actin and Glyceraldehyde 3-phosphate dehydrogenase (GAPDH). After analyzing the coding regions that we sequenced, we found a 96.7 percent nucleotide similarity between the house sparrow and the zebra finch for the genes explored. There was a 94.1 percent nucleotide similarity between the cliff swallow and the zebra finch genes. Common primers and known sequences of genes give us a tool to investigate the mechanism of the antiviral immune response of birds to BCRV and other arboviruses. Investigation of the genes that are expressed during infection in these bird species will help us understand how differences in antiviral responses can make some hosts more susceptible to diseases than others.
