PRRSV in MARC-145

Porcine reproductive and respiratory syndrome virus (PRRSV) causes devastating economic losses through complex immunopathology, yet the molecular mechanisms orchestrating host cell fate remain elusive. Here we performed temporal transcriptomic profiling of PRRSV-infected MARC-145 cells at 0, 12, 24, 36, 48, and 72 hours post-infection, revealing the dynamic and temporally coordinated regulation of distinct regulated cell death (RCD) pathways. We discovered that PRRSV employs a sophisticated temporal strategy. The ferroptosis-related modules responsible for regulating lipid peroxidation were largely downregulated, whereas cytoprotective elements were upregulated. Pathway scores remained negative up to approximately 48 h.p.i., gradually approaching neutrality by 72 h.p.i., suggesting that viral mechanisms may inhibit iron-dependent lethal lipid damage.