# PEDV and BVDV coinfection activates the NF-κB pathway by a TLR7-dependent mechanism

## TL;DR

This study shows that when two viruses infect pig cells together, they boost each other's replication by activating a key immune pathway.

## Contribution

The study identifies TLR7 as a critical mediator of NF-κB activation during PEDV and BVDV coinfection.

## Key findings

- BVDV preinfection enhances PEDV replication in PK15 cells.
- Coinfection activates NF-κB through TLR7, increasing inflammatory cytokine expression.
- The NF-κB p65 subunit translocates to the nucleus during coinfection.

## Abstract

In recent years, coinfections of porcine epidemic diarrhea virus (PEDV) with other enteric pathogens have been frequently observed in diarrheal piglets. However, the underlying mechanisms of pathogen–pathogen or pathogen–host interactions during such coinfections remain to be elucidated.

In this study, an in vitro coinfection test of bovine viral diarrhea virus (BVDV) and PEDV was performed on model cells established before to explore the effect of coinfection on PEDV replication. Additionally, we used small interfering RNA (siRNA) assay to explore the role of TLRs related to NF-κB signaling in response to PEDV and BVDV coinfection.

We found that after preinfection with BVDV, PEDV replicates faster and more easily in PK15 cells. Further analysis revealed that coinfection of PEDV and BVDV significantly induced NF-κB activity, leading to increased translocation of the NF-κB p65 subunit from the cytoplasm to the nucleus. Moreover, TLR7 was identified as a key pattern recognition receptor in this process, mediating NF-κB activation and promoting the expression of inflammatory cytokines.

These results suggest that synergistic interactions between PEDV and BVDV during coinfection may strongly activate the host immune system and enhance virus replication. This study provides new insights into the immune modulation mechanisms underlying viral coinfections.