This study investigates the therapeutic potential of BK1.3, a synthetic Evasin-derived peptide, in a murine model of Coxsackievirus B3 (CVB3)-induced viral myocarditis. Myocarditis, an inflammatory disease of the heart muscle, is often triggered by viral infections and driven by excessive immune cell infiltration, mediated by chemokines. BK1.3 selectively targets and inhibits key CC chemokines involved in inflammation, potentially mitigating immune-mediated cardiac damage while preserving essential host defense mechanisms. Beyond its impact on cardiac inflammation, CVB3 infection induces systemic effects, including metabolic disturbances and liver dysfunction. The liver plays a critical role in regulating energy homeostasis and immune responses during infection, making it essential to understand how CVB3 alters hepatic metabolism and whether BK1.3 treatment influences these changes. To explore the metabolic adaptations of the liver during CVB3 infection and under BK1.3 treatment, we conducted a comprehensive proteomic analysis of liver tissue. Our goal was to assess infection-induced changes in protein expression related to metabolism, as well as to determine the extent to which BK1.3 modulates these processes. To interpret the functional implications of the observed proteomic changes, we applied HepatoKin1, a computational liver metabolism model, integrating protein abundance data to simulate metabolic pathway activity. This approach provided insights into how viral infection reprograms hepatic metabolism and how targeted chemokine inhibition may affect these adapatations. The dataset offers a valuable resource for understanding systemic metabolic responses in murine viral myocarditis and evaluating the potential benefits of chemokine-targeted therapy.