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Mitochondrial dysfunction in PRRSV-2-infected macrophages.

Thien-Phong Vu Manh1, Alba Frias-De-Diego2, Abigail Williams2

  • 1Aix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.

Frontiers in Immunology
|October 31, 2025
PubMed
Summary
This summary is machine-generated.

Porcine reproductive and respiratory syndrome virus (PRRSV) infection impairs mitochondrial function in lung macrophages, with porcine alveolar macrophages (PAMs) showing greater impact than pulmonary intravascular macrophages (PIMs). This study reveals strain-specific responses to PRRSV-2 in swine.

Keywords:
NanoStringPRRSV-2macrophagesmitochondrial dysfunctionpigseahorse technologytranscriptomics

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Area of Science:

  • Veterinary Virology
  • Immunology
  • Cellular Metabolism

Background:

  • Porcine reproductive and respiratory syndrome virus (PRRSV) causes significant economic losses in the swine industry.
  • PRRSV infects lung macrophages, leading to compromised immune responses.
  • Understanding PRRSV-2 strain variations and their impact on macrophage function is crucial for disease control.

Purpose of the Study:

  • To investigate the metabolic and immune profiles of porcine alveolar macrophages (PAMs) and pulmonary intravascular macrophages (PIMs) infected with different PRRSV-2 strains.
  • To evaluate the impact of PRRSV-2 infection on mitochondrial function and oxidative stress in lung macrophages.
  • To identify differences in macrophage responses to distinct PRRSV-2 strains.

Main Methods:

  • Primary PAMs and PIMs were infected *in vitro* with North Carolina (NC) PRRSV-2 strains (NC134, NC174) and a prototype strain (VR2232).
  • Transcriptomic analysis (RNA-Seq) and gene expression validation (RT-qPCR, NanoString) were performed.
  • Functional assays (Seahorse) assessed mitochondrial respiration, while reactive oxygen species (ROS) and nitric oxide (NO) production were measured.

Main Results:

  • PRRSV-2 infection downregulated genes involved in oxidative phosphorylation and electron transport chain in PAMs.
  • PIMs exhibited limited transcriptomic alterations compared to uninfected cells.
  • PAMs showed a more substantial decrease in mitochondrial fitness than PIMs upon PRRSV-2 infection, consistent with transcriptomic data.
  • No significant differences in ROS or NO production were observed between infected and control macrophages.

Conclusions:

  • PRRSV-2 infection significantly alters mitochondrial function in lung macrophages, particularly PAMs.
  • Distinct PRRSV-2 strains can elicit different responses in lung macrophage subsets.
  • These findings offer insights into the pathogenesis of PRRSV-2 and highlight macrophage-specific responses to infection.