Circ-107191 Regulating Apoptosis by Sponging miR-34c to Enhance RAD54L Expression in PRRSV-Infected Boar Testes

Porcine reproductive and respiratory syndrome virus (PRRSV) is a major swine pathogen, causing reproductive issues in both sows and boars, significantly impacting the industry. This study investigates the molecular mechanisms of PRRSV-induced testicular damage in boars, focusing on the role of non-coding RNAs. Transcriptomic analysis of PRRSV-infected testes revealed significant alterations in mRNA, miRNA, lncRNA, and circRNA profiles, emphasizing the circ-107191/miR-34c/RAD54L regulatory axis. RAD54L is crucial for homologous recombination, and its decreased expression impairs DNA repair, leading to genetic damage accumulation and apoptosis. Using an ex vivo porcine testicular tissue culture model, we validated our findings and explored potential therapeutic interventions. Overexpression and knockdown experiments showed that dysregulation of this axis affects Sertoli cell and spermatogonia homeostasis, causing increased apoptosis, decreased proliferation, impaired blood-testis barrier formation, cytokine storms, and oxidative stress. PRRSV infection downregulates circ-107191, upregulates miR-34c, and reduces RAD54L levels, contributing to reproductive dysfunction. Our results suggest that targeting the circ-107191/miR-34c/RAD54L axis could alleviate PRRSV-induced testicular damage and preserve male fertility. This study provides novel insights into the role of non-coding RNAs in testicular function and spermatogenesis, offering potential therapeutic targets for addressing PRRSV-induced male infertility in swine and possibly translating to human reproductive health research.