Project description:While infection of chickens with highly pathogenic avian influenza (HPAI) H5N1 subtypes often leads to complete mortality within 24 to 48 h, infection of ducks in contrast causes mild or no clinical signs. Rapid onsets of fatal disease in chickens, but with no evidence of severe clinical symptoms in ducks, suggest underlying differences in their innate immune mechanisms. To understand the molecular basis for such difference, chicken and duck primary lung cells, infected with a low-pathogenicity avian influenza (LPAI) and two HPAI H5N1 viruses, were subjected to RNA expression profiling using Affymetrix Chicken GeneChip arrays. We used microarrays to analyze the gene expression profiles of primary chicken and duck lung cells infected with H2N3 LPAI and two H5N1 influenza virus subtypes to understand the molecular basis of host susceptibility and resistance. We have identified a set of key genes and pathways that could play an important role in mediating innate host resistance to avian influenza in chickens and ducks.
Project description:While infection of chickens with highly pathogenic avian influenza (HPAI) H5N1 subtypes often leads to complete mortality within 24 to 48 h, infection of ducks in contrast causes mild or no clinical signs. Rapid onsets of fatal disease in chickens, but with no evidence of severe clinical symptoms in ducks, suggest underlying differences in their innate immune mechanisms. To understand the molecular basis for such difference, chicken and duck primary lung cells, infected with a low-pathogenicity avian influenza (LPAI) and two HPAI H5N1 viruses, were subjected to RNA expression profiling using Affymetrix Chicken GeneChip arrays. We used microarrays to analyze the gene expression profiles of primary chicken and duck lung cells infected with H2N3 LPAI and two H5N1 influenza virus subtypes to understand the molecular basis of host susceptibility and resistance. We have identified a set of key genes and pathways that could play an important role in mediating innate host resistance to avian influenza in chickens and ducks. 24 hours following infection, total RNA from cells was extracted. Replicate RNA samples from each of the virus-infected (H2N3, H5N1 50-92, or H5N1 ty-Ty) or mock-infected chicken and duck cells (4 treatment groups for each species) were used for microarray analysis. Each of the RNA samples was hybridized to one GeneChipM-BM-. Chicken Genome Array (Affymetrix), and a total of 16 array chips were used.
Project description:H5N1 subtype highly pathogenic avian influenza virus has been spreading to Asia, Eurasia and African coutries. An original or six of recombinant H5N1 subtype influenza viruses with varying survivability were infected to chickens for elucidating genes correlated with pathogenicity.
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs.
Project description:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from ducks infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.
Project description:H5N1 subtype highly pathogenic avian influenza virus has been spreading to Asia, Eurasia and African coutries. An original or six of recombinant H5N1 subtype influenza viruses with varying survivability were infected to chickens for elucidating genes correlated with pathogenicity. Two chickens were infected with each 10^6EID50/ head virus intranasally, and their lung was collected from infected chicken at 24 hours after infection.
Project description:The pathogenesis of avian influenza A H5N1 virus in human has not been clearly elucidated. There have been increasing evidence suggesting a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. However, the role of aberrant innate immune response in human lungs infected by avian influenza H5N1 virus has not been explored and direct evidence for inappropriate innate responses in lungs of avian influenza H5N1 virus infected patients is lacking. In order to obtain evidences for the proposed role of aberrant innate immune response in avian influenza H5N1 virus pathogenesis in human, we analyzed expression profile of lung tissues from two fatal cases of avian influenza H5N1 virus infected patients in comparison to normal human lung using an expression microarray.
Project description:The mechanisms responsible for the molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or low pathogenic avian influenza virus (LPAIV) in avian species remain poorly understood. Thus, global immune response of chickens infected with HPAIV H5N1 (A/duck/India/02CA10/2011) and LPAIV H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAIV H5N1 induced excessive mRNA expression of cytokines (IFNA, OASL, MX1, RSAD2, IFITM5, GBP 1, IL1B, IL18, IL22, IL13, IL12B, CCL4, CCL9, CCL10, CX3CL1 etc) in lung tissues. This excessive cytokine response (cytokine storms) may cause tissue damage and high mortality in chickens. In contrast, the expression levels of most of the cytokines remained unchanged in the lungs of LPAIV H9N2 virus infected chickens. This study indicated the relationship between host cytokines response and their roles in pathogenesis in chickens infected with HPAIVs. Agilent Custom Chicken Gene Expression 8X60k (AMADID: G4102A_059389) designed by Genotypic Technology Private Limited , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
Project description:The pathogenesis of avian influenza A H5N1 virus in human has not been clearly elucidated. There have been increasing evidence suggesting a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. However, the role of aberrant innate immune response in human lungs infected by avian influenza H5N1 virus has not been explored and direct evidence for inappropriate innate responses in lungs of avian influenza H5N1 virus infected patients is lacking.