# Bta-miR-146b promotes infectious bovine rhinotracheitis virus replication and inhibits type I interferon expression via targeting IRAK1

## TL;DR

This study shows that a specific microRNA, bta-miR-146b, helps a virus infect cattle by weakening their immune response.

## Contribution

The novel finding is that bta-miR-146b promotes IBRV replication by inhibiting type I interferon via targeting IRAK1.

## Key findings

- bta-miR-146b expression is upregulated in IBRV-infected cells.
- bta-miR-146b promotes IBRV replication and inhibits type I interferon expression.
- IRAK1 is a direct target of bta-miR-146b, linking it to immune suppression.

## Abstract

Infectious bovine rhinotracheitis virus (IBRV) is a primary pathogen causing bovine respiratory disease syndrome. This virus can cause rhinotracheitis and vaginitis in cattle, resulting in high mortality and posing a serious threat to bovine production. MicroRNAs (miRNAs), a class of regulatory non-coding small RNAs, can modulate viral replication by influencing host immune responses. However, reports on the association between host miRNAs and IBRV infection are limited.

In this study, we screened differentially expressed miRNAs in MDBK cells after IBRV infection and determined that the expression of bta-miR-146b was significantly increased. We investigated the effects of bta-miR-146b on IBRV replication and its underlying molecular mechanisms using molecular biological techniques such as luciferase activity assays, Western Blot, and qRT-PCR, together with bioinformatics approaches.

We found that bta-miR-146b expression was up-regulated in IBRV-infected MDBK cells. Furthermore, transfection with bta-miR-146b mimics promoted IBRV replication in MDBK cells, whereas transfection with bta-miR-146b inhibitors inhibited IBRV replication, indicating that bta-miR-146b is a pro-infection factor. Additional studies showed that bta-miR-146b mimics inhibited type I interferon expression in MDBK cells, whereas its inhibitors enhanced it. Moreover, we identified IRAK1 as a direct target of bta-miR-146b and found that silencing IRAK1 expression rescued the effects of bta-miR-146b on viral replication and type I interferon expression.

These results suggest that bta-miR-146b regulates type I interferon expression and IBRV replication in MDBK cells by targeting IRAK1, and plays a key role in IBRV infection.