In the realm of poultry production, viral superinfections pose significant challenges, causing substantial economic losses worldwide. Among these, avian leukosis virus subgroup J (ALV-J) and infectious bursal disease virus (IBDV) are particularly concerning as they frequently lead to superinfections in chicken, further exacerbating production losses and health complications. Our previous research delved into the pathogenicity and immunosuppressive effects of these superinfections through in vitro and in vivo analyses. Yet, the underlying key genes and pathways governing this phenomenon remained elusive. In this study, we randomly selected three chickens at 21 days post infection from each treatment group (ALV-J, IBDV, ALV-J+IBDV, and control group) to collect the bursa of Fabricius samples for full transcriptome analysis. Utilizing these data, we constructed a comprehensive circRNA/lncRNA-miRNA-mRNA network which elucidated both synergistic and specific activations during the superinfection. Notably, three pivotal genes (FILIP1L, DCX, and MYPN) were pinpointed in datasets reflecting synergistic activations. Conversely, four other genes (STAP, HKR6, XKR4, and TLR5) emerged in datasets associated with specific activations. Further exploration revealed diverse significant GO terms and pathways associated with both synergistic and distinct activation processes. These ceRNA network and core genes potentially wield substantial influence over the synergistic or specific activation of tumorigenesis and pathogenesis induced by ALV-J and IBDV. These findings could help develop targeted therapies and improve disease control in poultry, reducing economic losses.
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http://dx.doi.org/10.3390/ani14233449 | DOI Listing |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11640342 | PMC |
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