Immunopathogenesis of lung lesions induced by the highly virulent Rosalía strain of PRRSV-1 circulating in Spain since 2020.

Rosalía PRRSV-1 causes severe lung disease through immune dysregulation and macrophage depletion.

This study characterizes the immunopathogenesis of severe lung disease induced by the highly virulent Rosalía strain of PRRSV-1 in experimentally infected piglets. The strain induced extensive interstitial pneumonia, proliferative and necrotizing pneumonia (PNP), and bronchopneumonia with marked endothelial activation and increased vascular permeability mediated by von Willebrand factor expression. Dynamic shifts in immune cell populations were observed throughout infection: at 10 days post-infection (dpi), T cells and calprotectin+ myeloid cells dominated lung infiltrates with marked depletion of CD163+ pulmonary alveolar macrophages; however, CD163+ septal macrophages infiltrated lesion areas. By 35 dpi, immune responses shifted toward adaptive immunity with CD163+ cell replenishment and significant CD20+ cell increases, including formation of tertiary lymphoid structures. These findings demonstrate that disease severity is characterized by immune dysregulation, including macrophage depletion, endothelial dysfunction, and delayed B-cell lymphoid responses, providing insights into pathogenic mechanisms of highly virulent PRRSV-1 strains.

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