A Multi-Omics Study of Chicken Infected by Nephropathogenic Infectious Bronchitis Virus

Abstract

Chicken gout resulting from nephropathogenic infectious bronchitis virus (NIBV) has become a serious kidney disease problem in chicken worldwide with alterations of the metabolic phenotypes in multiple metabolic pathways. To investigate the mechanisms in chicken responding to NIBV infection, we examined the global transcriptomic and metabolomic profiles of the chicken’s kidney using RNA-seq and GC–TOF/MS, respectively. Furthermore, we analyzed the alterations in cecal microorganism composition in chickens using 16S rRNA-seq. Integrated analysis of these three phenotypic datasets further managed to create correlations between the altered kidney transcriptomes and metabolome, and between kidney metabolome and gut microbiome. We found that 2868 genes and 160 metabolites were deferentially expressed or accumulated in the kidney during NIBV infection processes. These genes and metabolites were linked to NIBV-infection related processes, including immune response, signal transduction, peroxisome, purine, and amino acid metabolism. In addition, the comprehensive correlations between the kidney metabolome and cecal microbial community showed contributions of gut microbiota in the progression of NIBV-infection. Taken together, our research comprehensively describes the host responses during NIBV infection and provides new clues for further dissection of specific gene functions, metabolite affections, and the role of gut microbiota during chicken gout.

Evaluation of the reproductive system development and egg-laying performance of hens infected with TW I-type infectious bronchitis virus

“…Respiratory lesions, which are the most common pathogenic characteristic of IBV, subsequently recover and do not lead to the death of infected chickens [25,26]. Similar to QX-type strains, the renal lesions of urate deposition may be responsible for the death of chickens, although the mortality rate caused by TW I-type IBV was relatively low [27,28].…”

Low pathogenic avian influenza virus infection retards colon microbiota diversification in two different chicken lines

“…Studies in the chicken model have shown compositional changes in gut microbiota and differences in some of immune gene expression levels following H9N2 avian influenza virus (AIV), Newcastle disease virus (NDV) or infectious bronchitis virus (IBV) infection [ 29 – 32 ]. However, there are many environmental factors, such as age, breed, diet, housing, hygiene, and temperature that can also affect chicken microbiota [ 33 , 34 ] and thus might change the interactions between the host and viruses during the time of infection.…”

Evaluation of viral load and transcriptome changes in tracheal tissue of two hybrids of commercial broiler chickens infected with avian infectious bronchitis virus: a comparative study

“…Such understanding can provide invaluable insights into molecular pathogenesis in birds and various pathways involved in virus-host interactions. Recent advances in genomics, transcriptomics, proteomics, and metabolomics are now often incorporated into methodologies to analyze cellular and molecular interactions in biological systems [ 17 ].…”