Influenza transmission is shaped by temporary immunity, age-structured contact heterogeneity, and seasonal variation in transmissibility, generating persistent circulation, heterogeneous demographic burden, and recurrent epidemic activity. Yet the dynamical roles of these mechanisms are difficult to distinguish when they act simultaneously. We address this problem by combining endemic-equilibrium and threshold analysis, spectral-radius-based common-R0 calibration of regional contact systems, and phase-synchronized analysis of seasonally forced dynamics with background importation. The calibration fixes baseline invasion potential across 12 regional systems while retaining regional differences in contact-matrix eigenstructure and population composition. The homogeneous model shows that immunity waning changes the endemic infectious level without altering the invasion threshold. Under common-R0 calibration, the age-structured systems retain substantial differences in total and age-specific incidence. The 4–18-year age group contributes most strongly to the dominant transmission mode and exhibits the highest long-term annual incidence, ranging from 11.79% to 13.21% across the selected regions. Thus, a common baseline invasion potential does not imply equal total or age-specific epidemic burden when contact structure and population composition differ. Seasonal forcing replaces the time-independent age-structured endemic equilibrium with sustained recurrent epidemic trajectories and modifies epidemic magnitude, peak timing, and oscillatory behavior. Phase-synchronized Poincaré sections and Fourier spectra reveal an approximately biennial component, consistent with a subharmonic response to annual forcing. Together, these results show that contact structure and population composition determine epidemic burden beyond what is captured by R0 alone, whereas periodic forcing organizes recurrent epidemic timing in populations with temporary immunity.