Key result
Infection of porcine macrophages with ASFV strains caused early activation of antiviral defenses, followed by down-regulation of key inflammatory genes as viral replication progressed, particularly with the attenuated NH/P68 strain.
Why the study?
African swine fever virus has developed several strategies to replicate in porcine macrophages, but the modulation of antiviral genes across strains of diverse virulence remained to be characterized.
ASFV infection modulates antiviral gene expression in porcine macrophages, with down-regulation of inflammatory genes as replication progresses, highlighting potential immune evasion strategies.
Suggests ASFV immune-evasion targets in macrophages; leaves open validation for vaccine or antiviral development in swine.
African swine fever virus (ASFV), the aetiological agent of a devastating swine disease, has developed several strategies to replicate in porcine macrophages, its main target cells. In this work, we investigated the expression of 84 antiviral genes in macrophages infected with the virulent strain 26544/OG10 or the attenuated strain NH/P68. Infection with both strains caused an early activation of antiviral defenses, with up-regulation of RNA-sensing molecules and interferon-stimulating genes. However, as viral replication progresses, down-regulation of key inflammatory genes was observed, especially during infection with NH/P68, suggesting an impairment of macrophages' inflammatory response. Data generated provide a better portrait of ASFV immune evasion strategies.
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Franzoni et al. (2025) studied African swine fever virus infection (in vitro model) (n=4). ASFV virulent strain 26544/OG10 and attenuated strain NH/P68 vs. Mock-infected controls was evaluated on Expression of 84 antiviral genes (fold change relative to mock-infected control). Infection of porcine macrophages with ASFV strains caused early activation of antiviral defenses, followed by down-regulation of key inflammatory genes as viral replication progressed, particularly with the attenuated NH/P68 strain.
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