The goal of the study was to test the effects of an antibiotic substitute, plectasin, on the growth performance, immune function, intestinal morphology and structure, intestinal microflora, ileal mucosal layer construction and tight junctions, ileal immune-related cytokines, and blood biochemical indices of yellow-feathered chickens. A total of 1,500 one-day-old yellow-feathered chicks were randomly divided into four dietary treatment groups with five replicates in each group and 75 yellow-feathered chicks in each replication, as follows: basal diet (group A); basal diet supplemented with 10 mg enramycin/kg of diet (group B), basal diet supplemented with 100 mg plectasin/kg of diet (group C), and basal diet supplemented with 200 mg plectasin/kg of diet (group D). It was found that the dietary antimicrobial peptide plectasin could improve the ADG and had better F/G for the overall period of 1–63 days. Dietary plectasin can enhance H9N2 avian influenza virus (AIV) and Newcastle disease virus (NDV) antibody levels of yellow-feathered chickens at 21, and 35 days of age. Dietary plectasin can enhance the intestine structure, inhibit Escherichia coli and proinflammatory cytokines in the ileum, and ameliorate the blood biochemical indices of yellow-feathered chickens at 21 days of age. This study indicates that the antimicrobial peptide plectasin has beneficial effects on the growth performance, intestinal health and immune function of yellow-feathered chickens.

Since the chicken infectious anemia virus (CIAV) was discovered in 1979, which has been reported as an economically significant and immunosuppressive poultry disease in the world. A novel clinical detection method for the prevention and control of CIAV in the poultry sector is urgently needed. Here, we established a real-time recombinase-aided amplification assay (RAA) for CIAV on-site with a rapid, highly sensitive, strongly specific, low-cost, and simple operational molecular diagnosis detection method. The primers and probe were developed using the CIAV VP2 gene sequence, which has a 117-bp specific band. This assay, which could be carried out at 41°C and completed in 30 min without cross-reactivity with other viruses, had the lowest detection limit of 10 copies of CIAV DNA molecules per reaction. Furthermore, the kappa value of this assay was 0.947, the sensitivity was 93.33%, and the specificity was 100% when compared to the real-time quantitative polymerase chain reaction assay (real-time qPCR). These results indicate that using a real-time RAA assay to detect CIAV on-site could be beneficial. In the future, the real-time RAA test may be a regular assay for the prevention and control of CIAV, as well as help the reduction of economic losses in the poultry business.

Avian Leukosis Virus Subgroup J (ALV-J) is a tumorigenic virus with high morbidity and rapid transmission. N6-methyladenosine (m6A) is a common epigenetic modification that may be closely related to the pathogenicity of ALV-J. Currently, there are no reports on whether m6A modification is related to ALV-J induced tumor formation. In this study, we used methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) to examine the differences in m6A methylation and gene expression in normal livers and ALV-J-induced tumor livers systematically, with functional enrichment and co-expression analysis. The results identified 6,541 m6A methylated peaks, mainly enriched in CDS, and more than 83% of the transcripts contained 1-2 m6A peaks. For RNA-seq, 1,896 and 1,757 differentially expressed mRNAs and lncRNAs were identified, respectively. Gene enrichment analysis indicated that they may be involved in biological processes and pathways such as immunology-related and apoptosis. Moreover, we identified 17 lncRNAs, commonly existing in differently expressed methylome and transcriptome. Through co-expression analysis, 126 differentially expressed lncRNAs, and 18 potentially m6A-related methyltransferases were finally identified and connected, suggesting that m6A modifications might affect gene expression of lncRNAs and play a role in ALV-J induced tumor formation. This study provides the first comprehensive description of the m6A expression profile in tumor livers induced by ALV-J infection in chickens, which provides a basis for studying the role of m6A modification in ALV-J induced tumorigenesis. This study provides clues for studying the epigenetic etiology and pathogenesis of ALV-J.