Dissection of polygenic control of antibody response kinetics in adult chickens

The immune system plays an important role in protecting poultry from diseases. Understanding genetic control of immune response can be utilized to improve chicken health. Adult F2 hens were generated by mating highly inbred males of two MHC-congenic Fayoumi lines with G-B1 Leghorn hens. Antibody response after Salmonella enteritidis (SE) vaccination at day 10, and sheep erythrocyte (SRBC) and killed Brucella abortus (BA) immunizations at 19 and 22 weeks were measured. Agglutinating antibody titer at 7 day after primary immunization and mean titer of the final three samples (day 18, 32, and 63 after 2nd immunization) were used as parameters for primary and equilibrium phases, respectively. Secondary phase parameters of minimum (Ymin), maximum titers (Ymax) and time needed to achieve minimum (Tmin) and maximum (Tmax) titers were estimated from seven post-secondary titers using a nonlinear regression model. Both candidate gene and genome scan approaches were used to identify quantitative trait loci (QTL) affecting antibody response to SE vaccination and antibody response kinetics to SRBC and BA. Using the genome scan approach, QTL affecting immune response to SRBC and BA were detected by a stepwise process that culminated in interval mapping. Five significant QTL were detected at the 5% chromosome-wise level on chicken chromosomes 3, 5, 6 and Z, suggesting that regions on chromosomes 3, 5, 6 and Z contain QTL affecting antibody kinetics to SRBC and BA. Single nucleotide polymorphisms (SNP) of 15 immunity related genes were identified. Interferon-gamma, immunoglobulin light chain, interleukin-2, MHC class I alpha1, alpha2, class II beta1, and transforming growth factor-beta 2, 3 and 4 SNP were significantly associated with antibody responses to SE vaccination or antibody response kinetics to SRBC and BA or both. For some candidate genes, significant associations were primarily detected in the lineage of the M5.1 grandsire, but in that of the M15.2 grandsire on the others. Strong interactions of the MHC with candidate genes on antibody response were indicated from the study. All the genes characterized in the present study are, therefore, strong potential candidates for application in marker-assisted selection to improve vaccine response and immunocompetence in chickens

Genes for Skeletal Strength in Poultry

A unique resource population was used to determine that variation in a gene of the bone morphogenetic protein (BMP) family is associated with shank measurements in poultry. Knowledge of genetic variation and associations with traits related to skeletal integrity will enable genetic selection of poultry populations for stronger bones, thus reducing bone breakage in the live animal and on the processing line

Overexpression of Chicken IRF7 Increased Viral Replication and Programmed Cell Death to the Avian Influenza Virus Infection Through TGF-Beta/FoxO Signaling Axis in DF-1

During mammalian viral infections, interferon regulatory factor 7 (IRF7) partners with IRF3 to regulate the type I interferon response. In chickens, however, it is still unclear how IRF7 functions in the host innate immune response, especially given that IRF3 is absent. To further elucidate the functional role of chicken IRF7 during avian influenza virus (AIV) infection, we generated inducible IRF7 overexpression DF-1 cell lines and performed in vitro infection using low pathogenic AIVs (LPAIVs). Overexpression of IRF7 resulted in higher viral replication of H6N2 and H10N7 LPAIVs compared to empty vector control cells regardless of IRF7 expression level. In addition, a high rate of induced cell death was observed due to elevated level of IRF7 upon viral infection. RNA-seq and subsequent transcriptome analysis of IRF7 overexpression and control cells discovered candidate genes possibly controlled by chicken IRF7. Functional annotation revealed potential pathways modulated by IRF7 such as TGF-beta signaling pathway, FoxO signaling pathway and cell structural integrity related pathways. Next, we analyzed the host response alteration due to the IRF7 overexpression and additionally discovered the possible connection of chicken IRF7 and JAK-STAT signaling pathway. These findings suggest that chicken IRF7 could modulate a wide range of cellular processes in the host innate immune response thus meticulous control of IRF7 expression is crucial to the host in response to AIV infection

Infection of Commercial Laying Hens with Newcastle Disease Virus: Differing Responses between Birds Provide Potential for Genetic Improvement through Selection

Exotic Newcastle Disease Virus (ENDV) cause extremely rapid mortality in chickens after exposure to the virus. People rely heavily on poultry to provide protein and income in many places where NDV is not effectively controlled through vaccination and biosecurity. Losses from NDV contribute to worldwide hunger and poverty. It may be possible to use genetic selection to produce chickens that have a stronger immune response in the face of NDV challenge. For genetic selection to be successful, two major elements are required: differences in immune response among chickens and genetic control of these differences. This study clearly demonstrated the existence of both these factors. These findings demonstrate the feasibility of genetic selection to produce chickens that are more resistant to NDV and thereby lessen the burdens of hunger and poverty

Genetics and Genomic Regions Affecting Response to Newcastle Disease Virus Infection under Heat Stress in Layer Chickens.

Newcastle disease virus (NDV) is a highly contagious avian pathogen that poses a tremendous threat to poultry producers in endemic zones due to its epidemic potential. To investigate host genetic resistance to NDV while under the effects of heat stress, a genome-wide association study (GWAS) was performed on Hy-Line Brown layer chickens that were challenged with NDV while under high ambient temperature to identify regions associated with host viral titer, circulating anti-NDV antibody titer, and body weight change. A single nucleotide polymorphism (SNP) on chromosome 1 was associated with viral titer at two days post-infection (dpi), while 30 SNPs spanning a quantitative trait loci (QTL) on chromosome 24 were associated with viral titer at 6 dpi. Immune related genes, such as CAMK1d and CCDC3 on chromosome 1, associated with viral titer at 2 dpi, and TIRAP, ETS1, and KIRREL3, associated with viral titer at 6 dpi, were located in two QTL regions for viral titer that were identified in this study. This study identified genomic regions and candidate genes that are associated with response to NDV during heat stress in Hy-Line Brown layer chickens. Regions identified for viral titer on chromosome 1 and 24, at 2 and 6 dpi, respectively, included several genes that have key roles in regulating the immune response

Commercial Layer-type Chickens and Newcastle Disease Virus Infection:Toward Genetic Selection of More Resilient Chickens

Exotic Newcastle Disease Virus(NDV)causes major losses due to extremely quickmortalityin chickensafter exposure to the virus. In places where this virusis not effectively controlled through vaccination and biosecurity, people rely heavily on poultry to provideprotein and income.Losses from NDV contributeto worldwide hunger and poverty. It may be possible to use genetic selection to produce chickens thatnot onlyhave a stronger immune response in the face of NDV challengebut also respond better to vaccination. In order for genetic selection to be successful,two major elements are required: differences in immune response between chickens and genetic control of these differences. This study clearly demonstrates the existence of both these factors.These findings provide strong possibility for the ability of genetic selection to produce chickens that are more resistant to NDV and thereby lessen the burdens of hunger and poverty