Nipah virus (NiV) is a sporadic but highly lethal zoonotic pathogen, with case fatality rates of 40%-75% in affected regions. Prolonged incubation, documented relapse, and delayed-onset encephalitis following apparent recovery suggest that NiV dynamics are shaped by complex temporal processes.
However, mechanistic contributions of these processes to epidemic persistence remain poorly understood.
In this study, we develop and analyze a delay differential equation model for NiV transmission that explicitly incorporates incubation delay, relapse, and post-recovery delay effects. We compute a primary-transmission reproduction threshold (R0), characterize the disease-free and endemic equilibria, and analyze their stability, including delay-induced Hopf bifurcations. We show that relapse modifies the endemic persistence condition and existence of an endemic equilibrium is not determined by the classical primary-transmission threshold R0 = 1. We calibrate the model to NiV incidence data from Bangladesh (2001-2024) and perform simulations and sensitivity analyses to evaluate the effects of relapse and delays across epidemiological scenarios. Results indicate that sustained oscillations occur only under hypothetical parameter regimes, suggesting that delay-induced periodic outbreaks are unlikely under empirically informed conditions. Scenario analyses show that relapse and encephalitis related delays primarily affect post-peak dynamics, whereas incubation delay modulates the timing and magnitude of the outbreak peak. We also introduce a relapse-driven replenishment fraction to quantify contribution of relapse to continued transmission, demonstrating its increasing importance after the primary outbreak peak. Overall, our findings identify relapse as a key mechanism for epidemic persistence and underscore the importance of incorporating relapse and biological time delays into epidemiological modeling and public health strategies.