Infection with causes aberrant expression of host microRNAs (miRNAs)， and normalizing the levels of dysregulated miRNAs can attenuate pathology. Here， we show that the host miRNA， ， is markedly upregulated during the progression of hepatic schistosomiasis. We demonstrate that elevation of induces hepatic fibrosis in infected mice by suppressing the expression of its target gene， . We show that infection with induces the expression of transforming growth factor β1 (TGF-β1)， which in turn upregulates the expression of through SMAD2/3-DROSHA-mediated post-transcriptional regulation. Furthermore， inhibition of with recombinant adeno-associated virus 8 (rAAV8)-mediated delivery of Tough Decoy RNAs in mice attenuated hepatic fibrosis and prevented lethality following schistosome infection. Taken together， our data highlight the potential for rAAV8-mediated inhibition of as a therapeutic strategy to treat hepatic schistosomiasis.