Zhang Qinchuan, Zhang Manyi, Qi Xiao, Sheng Jinliang, Sun Yanming, Zhang Yanbing
College of Animal Science and Technology, Shihezi University, Shihezi, 832003, China.
Xinjiang Production & Construction Corps Key Laboratory of Animal Biomedicine, Tumushuke, 843900, China.
Biochem Genet. 2025 Feb 19. doi: 10.1007/s10528-025-11054-x.
Porcine reproductive and respiratory syndrome (PRRS) is one of the most economically devastating diseases affecting the global pig industry. Host microRNAs directly target viral gene regions to exert their disease-fighting effects. PRRS virus (PRRSV) infection upregulates miR-361-3p expression; however, it is unclear whether it can exert inhibitory effects by directly targeting viral genes. Bioinformatic and experimental findings revealed that miR-361-3p inhibited PRRSV replication by directly targeting the PRRSV ORF1b and ORF1a loci. Intramuscular injection of pcDNA3.1-pri-miR-361 verified the expression of miR-361-3p in mammals. In summary, miR-361-3p plays an important role in infection and may be a promising therapeutic target for PRRS, providing insights into possible drug therapies.
猪繁殖与呼吸综合征（PRRS）是影响全球养猪业的最具经济破坏力的疾病之一。宿主微小RNA直接靶向病毒基因区域以发挥其抗病作用。PRRS病毒（PRRSV）感染会上调miR-361-3p的表达；然而，尚不清楚它是否能通过直接靶向病毒基因发挥抑制作用。生物信息学和实验结果表明，miR-361-3p通过直接靶向PRRSV ORF1b和ORF1a基因座抑制PRRSV复制。肌肉注射pcDNA3.1-pri-miR-361证实了miR-361-3p在哺乳动物中的表达。总之，miR-361-3p在感染中起重要作用，可能是PRRS的一个有前景的治疗靶点，为可能的药物治疗提供了思路。
