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<p>Akabane virus (AKAV), the etiological agent of Akabane disease, is known to induce congenital malformations and neuropathologies in the fetuses of pregnant cattle and sheep. To analyze the changes in gene expression patterns that occur in AKAV-infected cells, two types of primary bovine cells – primary bovine testicular Sertoli cells (BTSCs) and primary bovine joint synovial cells (BJSCs) – were selected. These cells were confirmed to be infected by AKAV strain TJ2016. Subsequently, RNA-sequencing technology was employed to analyze the transcriptomic profiles of AKAV-infected BTSCs and BJSCs, as well as Madin-Darby ovine kidney (MDOK) cells. The AKAV-infected cells exhibited activation of antiviral signaling pathways. Notably, there was upregulation of the expression levels of interferon-stimulated genes, as well as genes related to inflammation and cytokines. IL-1β, TNF-α, CXCL8, CCL2, and Rnd1 were found to be significantly upregulated in AKAV-infected cells. Moreover, Rnd1 was found to inhibit the replication of AKAV. Because TNF-α plays an important role in the induction of Rnd1, this provides additional evidence for the regulation and function of Rnd1.</p>

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Transcriptomic analysis reveals Rnd1 to be a key player in antiviral immunity against Akabane virus via the TNF-α pathway

  • 期刊论文

  • 发表日期：

    2025年11月28日

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  • Dongjie Chen,
  • Jingjing Wang,
  • Chao Sun,
  • Fang Wei,
  • Shengkui Xu,
  • Ruyang Yu,
  • Shaoqiang Wu

摘要

Akabane virus (AKAV), the etiological agent of Akabane disease, is known to induce congenital malformations and neuropathologies in the fetuses of pregnant cattle and sheep. To analyze the changes in gene expression patterns that occur in AKAV-infected cells, two types of primary bovine cells – primary bovine testicular Sertoli cells (BTSCs) and primary bovine joint synovial cells (BJSCs) – were selected. These cells were confirmed to be infected by AKAV strain TJ2016. Subsequently, RNA-sequencing technology was employed to analyze the transcriptomic profiles of AKAV-infected BTSCs and BJSCs, as well as Madin-Darby ovine kidney (MDOK) cells. The AKAV-infected cells exhibited activation of antiviral signaling pathways. Notably, there was upregulation of the expression levels of interferon-stimulated genes, as well as genes related to inflammation and cytokines. IL-1β, TNF-α, CXCL8, CCL2, and Rnd1 were found to be significantly upregulated in AKAV-infected cells. Moreover, Rnd1 was found to inhibit the replication of AKAV. Because TNF-α plays an important role in the induction of Rnd1, this provides additional evidence for the regulation and function of Rnd1.