MiR-22 promotes porcine reproductive and respiratory syndrome virus replication by targeting the host factor HO-1

- PRRSV infection induces miR-22 expression.
- MiR-22 directly interacts with the antiviral host factor HO-1.
- Expression levels of HO-1 and miR-22 are inversely correlated.
- MiR-22 promotes PRRSV replication by targeting the antiviral host factor HO-1.

Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important viruses affecting the swine industry worldwide. MicroRNAs (miRNAs) play vital roles in virus-host interactions by regulating the expression of viral or host gene at posttranscriptional level. Our previous research showed that PRRSV infection down-regulates the expression of heme oxygenase-1 (HO-1), a pivotal cytoprotective enzyme, and overexpression of HO-1 inhibits PRRSV replication. In this study, we demonstrate that host miRNA miR-22 can downregulate HO-1 expression by directly targeting its 3′ untranslated region. Suppression of HO-1 expression by miR-22 facilitates PRRSV replication. This work suggests that PRRSV may utilize cellular miRNA to modify antiviral host factor expression, enabling viral replication, which not only provides new insights into virus-host interactions during PRRSV infection, but also suggests potential therapies for PRRSV infection.