This article is part of the supplement: Proceedings of the International Symposium on Animal Genomics for Animal Health (AGAH 2010)
Genomic study of the response of chicken to highly pathogenic avian influenza virus
1 Parco Tecnologico Padano, 26900 Lodi, Italy
2 Animal Health Department, Istituto Zooprofilattico Sperimentale della Lombardia e dell'Emilia Romagna “Bruno Ubertini”, 25124 Brescia, Italy
3 CAAS-ILRI Joint Laboratory on Livestock and Forage Genetic Resources, Institute of Animal Science, Chinese Academy of Agricultural Sciences (CAAS), Beijing, 100193, PR China
4 Institute of Farm Animal Genetics, Friedrich Loeffler Institut, Mariensee, D-31535, Germany
5 DIPAV, Università degli Studi di Milano, 20133 Milano, Italy
6 IBBA-CNR, 26900 Lodi, Italy
BMC Proceedings 2011, 5(Suppl 4):S25 doi:10.1186/1753-6561-5-S4-S25Published: 3 June 2011
The host mounts an immune response to pathogens, but few data are currently available on the role of host genetics in variation in response to avian influenza (AI). The study presented here investigated the role of the host genetic background in response to in vivo infection with AI virus (AIV).
Experimental lines of chicken and commercial crosses were experimentally infected intratracheally with 103 EID50/bird of A/Chicken/Italy/13474/99 H7N1 highly pathogenic avian influenza virus (HPAIV). Chickens were genotyped for the Mx polymorphism causing the S631N mutation, and for the Major Histocompatibility Complex (MHC). Whole-genome genotyping was carried out using 60 k Single Nucleotide Polymorphism (SNP) array developed by the poultry Genome-Wide Marker-Assisted Selection Consortium (GWMASC).
Variability in response of different chicken lines to the HPAIV infections and some degree of resistance to AI were observed: a statistically significant effect of chicken line on the response to infection was found. There was no association between survival in healthy conditions and polymorphisms at the Mx gene and the MHC-B region. The analysis based on the 60 k SNPs provided a good clustering of the chicken lines, but no specific genetic cluster associated with response to AIV was identified.
Neither the genotype at the Mx gene or MHC-B locus, nor for SNP spanning the whole-genome identified loci involved in variations to response to AIV infection. These results point towards the possibility that either the genetic factors affecting the response of chickens to the H7N1 HPAIV are weak, or relevant alleles were not segregating in the studied populations.