Model showing the orchestration of viral trafficking in late steps of the HCV life cycle by AP complexes and their regulators. HCV hijacks the AP-1A, AP-1B, AP-2, and AP-4 complexes to mediate intracellular traffic of viral particles in temporally distinct late steps of its life cycle. Host kinases AAK1 and GAK regulate the assembly and release of cell-free- and cell-to-cell-transmitted virus through phosphorylation of AP-1 (green and yellow) and AP-2 (pink). Sunitinib, erlotinib, and selective inhibitors of AAK1 and GAK disrupt these temporally distinct steps of the viral life cycle.