Porcine reproductive and respiratory syndrome virus downregulates the circ-107191/miR-34c/RAD54L axis to promote testicular cell apoptosis via impaired homologous recombination repair.

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection impairs male reproductive function, causing substantial economic losses. This study investigates PRRSV-induced testicular dysfunction through transcriptomic analysis, identifying 463 circRNAs, 50 miRNAs, and 4627 mRNAs that are differentially expressed in infected testes. Functional enrichment analysis underscores the role of the circRNA-miRNA-mRNA network in immune responses, apoptosis, and germ cell maintenance. The circ-107191/miR-34c/RAD54L axis emerges as a pivotal pathway: PRRSV infection reduces circ-107191, which enhances miR-34c activity and suppresses RAD54L expression, thereby exacerbating apoptosis and oxidative stress. Ex vivo porcine testicular models demonstrate that decreased circ-107191 or elevated miR-34c levels disrupt blood-testis barrier integrity, increase inflammation and apoptosis, and suppress testosterone production. Restoring circ-107191 expression or inhibiting miR-34c mitigates tissue damage, enhances cell proliferation, reduces oxidative stress, and stabilizes endocrine function. These findings highlight the circ-107191/miR-34c/RAD54L axis as a potential therapeutic target for PRRSV-induced male infertility, providing novel insights into ncRNA-mediated reproductive regulation.