Transcriptomic Analysis Reveals Rnd1 as a Key Player in Antiviral Immunity Against Akabane virus via TNF-α pathway

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 comprehensively analyze the protein alterations and precisely elucidate the molecular mechanism in AKAV-susceptible cells, two types of primary bovine cells, namely primary bovine testicular sertoli cells (BTSC) and primary bovine joint synovial cells (BJSC), were selected. These cells were confirmed to be effectively infected by the AKAV TJ2016 strain. Subsequently, RNA-sequencing technology was employed to further analyze the transcriptomic profiles of AKAV-infected BTSC, BJSC, and MDOK cells. The molecular features of AKAV-infected cells demonstrated a remarkable activation of antiviral signaling pathways. Notably, there was an upregulation in the expression levels of interferon-stimulated genes, as well as genes related to inflammation and cytokines. Through a comparison between infected and non-infected cells, it was revealed that IL-1β, TNF-α, CXCL8, CCL2 and Rnd1 were significantly up-regulated in AKAV-infected cells. Moreover, Rnd1 was found to inhibit the replication of AKAV and TNF-αplays an important role in the induction of Rnd1, which provides additional evidence for the regulation and function of Rnd1.