# Phospholipase PLA2G16 Accelerates the Host Interferon Signaling Pathway Response to FMDV

## TL;DR

This study shows that PLA2G16 boosts the host's antiviral immune response to Foot-and-Mouth Disease Virus by enhancing interferon signaling.

## Contribution

The novel finding is that PLA2G16 specifically promotes an innate immune response against FMDV.

## Key findings

- PLA2G16 overexpression increases phosphorylated STAT1 and interferon-stimulating factors during FMDV infection.
- PLA2G16 helps the host detect FMDV nucleic acid early and activate the interferon signaling pathway.
- Supernatants from PLA2G16-overexpressing cells stimulate antiviral responses in uninfected cells.

## Abstract

PLA2G16 is a member of the phospholipase A2 family that catalyzes the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. Previously, PLA2G16 was found to be a host factor for picornaviruses. Here, we discovered that the Foot-and-Mouth Disease Virus (FMDV) infection led to an elevation in PLA2G16 transcription. We established PLA2G16 overexpression and knockdown cell lines in PK-15 cells to investigate the potential role of PLA2G16 in FMDV infection. Our findings revealed that during FMDV infection, PLA2G16-overexpressing cells had increased levels of phosphorylated STAT1 and the interferon-stimulating factors ISG15 and ISG56. In PLA2G16-overexpressing cells, p-STAT1 was observed at higher levels and earlier than in wild-type cells. Subsequent research demonstrated that PLA2G16 specifically promoted an antiviral innate immune response against FMDV. The host could detect the early release of FMDV viral nucleic acid in PLA2G16-overexpressing cells and trigger the interferon signaling pathway. Additionally, we discovered that the supernatants of PLA2G16-overexpressing cells stimulated the production of higher levels of ISG56 and phosphorylated STAT1. This suggests that PLA2G16-overexpressing cells can activate the innate immune pathway of uninfected cells after FMDV infection.