# Differential Effects of Selenium Compounds on Mitochondrial Function in PRRSV-Infected Porcine Alveolar Macrophages

## TL;DR

This study explores how different forms of selenium affect mitochondrial function in pig immune cells infected with a virus, finding that selenium improves energy production but does not directly fight the virus.

## Contribution

The study reveals that DL-selenomethionine enhances mitochondrial ATP production in PRRSV-infected macrophages without showing antiviral effects.

## Key findings

- DL-selenomethionine increased glycolytic and mitochondrial ATP production in infected cells.
- Selenium compounds did not show antiviral activity against PRRSV in vitro.
- Transcriptome analysis showed upregulation of genes like IL6, IL8, and MX1 during infection, but selenium had no significant effect.

## Abstract

Selenium (Se) is a trace mineral with antioxidant and anti-inflammatory properties. Se deficiency increases oxidative stress and immunosuppression. In swine, dietary Se supplementation enhances immunity and growth, and previous studies suggest it protects immune cells during viral infection. Porcine reproductive and respiratory syndrome virus (PRRSV) causes severe respiratory and reproductive failure in swine, resulting in annual losses of 1.2 billion USD. Vaccine efficacy is hampered by the virus’s high mutation rate, requiring alternative approaches. This study examines the effects of organic (DL-Selenomethionine, L-Selenomethionine, yeast-selenium) and inorganic (sodium selenite) Se on PRRSV infection in vitro. Porcine alveolar macrophages, the primary target of PRRSV in the lung, were isolated from healthy animals and infected with PRRSV-2 with or without Se. Mitochondrial function, gene expression, oxidative stress, and viral load were assessed post-infection. DL-selenomethionine showed increased glycolytic and mitochondrial ATP production relative to other compounds, suggesting improved mitochondrial function. No antiviral activity against PRRSV was observed. Transcriptome analysis revealed infection-driven modulation, with upregulation of IL6, IL8, IL1B1, MX1, and TXNRD1, but Se had no significant effect. While Se did not exhibit antiviral activity in vitro, its enhancement of mitochondrial function offers additional insight supporting its potential immunomodulatory benefits observed in previous in vivo studies.