Abstract
Feline viral rhinotracheitis is a prevalent disease among cats caused by feline herpesvirus 1 (FHV-1). microRNAs (miRNAs), which serve as important regulatory factors in the host, participate in the regulation of the host innate immune response to virus infection. However, the roles of miRNAs in the FHV-1 life cycle remain unclear. In this study, we found that a new miRNA, miR-101, could suppress FHV-1 replication. FHV-1 infection upregulated the expression level of miR-101 in a cGAS-dependent manner. Furthermore, miR-101 could significantly enhance type I interferon antiviral signaling by targeting suppressor of cytokine signaling 5 (SOCS5), a negative regulator of the JAK-STAT pathway. Likewise, knockdown of cellular SOCS5 also suppressed FHV-1 replication due to the enhancement of IFN-I-induced signaling cascades. Taken together, our data demonstrated a new strategy for miR-101-mediated defense against FHV-1 infection by enhancing IFN-I antiviral signaling and increased the knowledge of miRNAs regulating innate immune signaling pathways.
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