The Mechanism Underlying The Multiplication Of SCRV In CPB Cells Regulated By MiR-122

Siniperca chuatsi rhabdovirus(SCRV)infection has caused great economic loss to snakehead fish culture in China,and there aren't any efficient preventive and therapeutic ways.MicroRNA is a class of small non-coding RNA that plays an important role in the regulation of virus infection.Our previous research indicates that MicroRNA-122(miR-122)was up regulated in CPB cells upon SCRV infection,overexpression of miR-122 mimic promoted the replication of SCRV.Therefore,this project aims at illuminating the regulatory role of miR-122 in CPB cells upon SCRV infection.The main studies included:(1)MiR-122 promote the proliferation of SCRVWe identified that SCRV infection up-regulated the expression of miR-122 in CPB cells.Notably,transfecting with miR-122 mimic significantly promote SCRV replication.MiR-122 inhibitor can significantly inhibit SCRV replication.(2)MiR-122 regulates SCRV proliferation by targeting host genes.Interforn regulatory factor-1(IRF-1)was identified as the target gene of miR-122.Interestingly,knockdown of IRF-1 by siRNA,similar to the overexpression of miR-214,can stimulate SCRV replication and inhibit IFN-? production.Furthermore,we found that siIRF1-1-mediated promotion of SCRV replication could be restored by knockdown of cellular miR-122,indicating that miR-122 stimulate SCRV replication by targeting to IRF-1.Together with our previous report that miR-122 was up-regulated upon SCRV infection,we proposed a model: SCRV infection up-regulated miR-122,the up-regulated miR-122 decreased the expression of its target gene IRF-1,which reduced IFN-? production and therefore promoted SCRV replication.This study provides a better understanding of the molecular mechanisms on the pathogenesis of SCRV and a potential antiviral strategy against SCRV infection.