Key result
Overexpressing miR-9041 and miR-9850 promotes WSSV replication by suppressing STAT and downstream dynamin genes.
p-value: p=<0.01
Host miRNAs miR-9041 and miR-9850 enhance WSSV replication in shrimp by suppressing the JAK/STAT pathway and downstream dynamin genes.
Hypothesis-generating for miRNA-based WSSV control in aquaculture; leaves open validation in mammalian systems.
MicroRNAs (miRNAs) have important roles in post-transcriptional regulation of gene expression. During viral infection, viruses utilize hosts to enhance their replication by altering cellular miRNAs. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway plays crucial roles in the antiviral responses. In this study, two miRNAs (miR-9041 and miR-9850) from Macrobrachium rosenbergii were found to promote white spot syndrome virus (WSSV) replication. The up-regulation of miR-9041 or miR-9850 suppresses STAT expression in the gills of M. rosenbergii, which subsequently down-regulates the expression of its downstream dynamin (Dnm) genes: Dnm1, Dnm2, and Dnm3. Knockdown of miR-9041 and miR-9850 restricts WSSV replication by up-regulating STAT and Dnm gene expression. The silencing of STAT, Dnm1, Dnm2, or Dnm3 led to an increase of the number of WSSV copies in shrimp. The injection of recombinant Dnm1, Dnm2, or Dnm3 proteins could inhibit WSSV replication in vivo. Overall, our research indicates the roles of host miRNAs in the enhancement of WSSV replication by regulating the host JAK/STAT pathway.
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Huang et al. (2016) studied White spot syndrome virus (WSSV) infection. miR-9041 and miR-9850 overexpression or knockdown vs. Scrambled miRNAs or WSSV only was evaluated on WSSV copies (viral replication) (p=<0.01). Overexpression of host miR-9041 and miR-9850 promoted WSSV replication by suppressing the host STAT gene and its downstream dynamin genes, while their knockdown restricted viral replication.
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