ArticleIn vitro cellular & developmental biology. Animal2018
Identification of key genes fluctuated induced by avian leukemia virus (ALV-J) infection in chicken cells.
Article in In vitro cellular & developmental biology. Animal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Deciphering host-virus interaction networks in ALV infection: an integrative multi-omics perspective.Frontiers in immunology · 2026Review
- CCL4 participates in the reprogramming of glucose metabolism induced by ALV-J infection in chicken macrophages.Frontiers in microbiology · 2023Article
- Review
- Clonal anergy of CD117Retrovirology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Avian leukemia subgroup J (ALV-J) is one of the most detrimental neoplastic diseases in poultry production. However, the differences between somatic cells and immune cells post-infection remain poorly understood. The aim of our study was to detect the different responses in chicken to infection with ALV-J in different cell lines. In this study, we detected transcriptome expression changes during infection with ALV-J in chicken embryo fibroblast (CEF) and HD11 cell lines. RNA-Seq was used to determine the expression levels of mRNA transcripts from the two cell types after infection with ALV-J at 1, 4, and 7 dpi, and gene ontology analyses were used to cluster differentially expressed genes into pathways. Quantitative real-time PCR confirmed the expression of 336 and 269 differentially expressed genes in CEF and HD11 lines, respectively, involved in innate immunity (OASL, CCL4), adaptive immunity (LYZ, CD72), apoptosis and autophagy (WISP2, COMP), inflammation (JSC, IL8), and tumorgenesis (PCNA, GPX3). The notable signal transduction pathways included the PPARs signaling pathway and ECM-receptor interactions in CEF, and the Toll-like receptor, NOD-like receptor, and RIG-I-like receptor signaling pathways in HD11. To our knowledge, this is the first study to use high-throughput sequencing methods to investigate viral infection in different cell types. The results of the present study form a foundation for developing potential biological markers for viral infection.
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Registered trials
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