Evolving Social Context Regulates Contagion Spread in Multiplex Networks
Contagion processes across biological, behavioral, and informational systems are shaped not only by transmission dynamics, but also by adaptive social responses emerging through human interactions. Understanding how social context regulates contagion spread is therefore critical for characterizing real-world spreading processes. Yet standard epidemic models often focus primarily on contagion states, treating social context as static or only weakly coupled to transmission. Here, we develop a multiplex-network framework that couples contagion dynamics with co-evolving social context. Unlike classical threshold contagion models, which apply thresholds directly to contagion prevalence or adoption states, our framework applies heterogeneous local and global thresholds to evolving context dynamics. The model further captures context-mediated transmission through targeted spread, in which contagion selectively propagates toward the locally most context-vulnerable susceptible individual. This contrasts with broadcast transmission, where spreading effort is distributed uniformly across susceptible neighbors. We show that coupling contagion with evolving context fundamentally reshapes spreading dynamics, producing delayed convergence and non-monotonic final prevalence. Targeted and broadcast transmission mechanisms exhibit distinct sensitivities to local and global social responses, highlighting tradeoffs in intervention strategies. We further show that co-evolving context can generate resilience by slowing propagation and delaying equilibrium, while pre-existing social resilience can substantially suppress contagion even under high transmission rates. These results suggest that contagion outcomes can vary substantially as a function of evolving social response and pre-existing social resilience. SignificanceContagion outcomes are often shaped before transmission begins. Existing social environments can make populations more vulnerable or more resistant to future spread, yet this latent resilience is difficult to capture when interventions are represented only as changes to contact or transmission rates. Our results show that social context can act as a regulatory mechanism that suppresses and delays contagion spread. In particular, prior pro-social alignment can create resilience before exposure occurs, helping explain why community prevention, peer support, and reintegration programs may alter contagion outcomes even when they do not directly target the transmission process.