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Although p53 signaling was activated in both clones, the specific expression patterns of downstream effector genes diverged—such as the upregulation of Gpc4 in BHK-7—implying that the initial mutagenic event induced long-term reprogramming of cell fate and stress response pathways ( A systems-level model of mutagenesis-driven bipolarization of viral replication and its validation To integrate these multi-layered findings, we developed a comprehensive systems-level model illustrating how heavy-ion mutagenesis drives the polarization of antiviral outcomes in BHK-5 and BHK-7 clones ( Figure 10 )