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• To demonstrate the Galerkin method's validity, via the accuracy of its predictions using DPDE models. • To structure a process for applying the theoretical framework to find theoretical results. • To show the impacts of diffusion and immune response delay on the model, through bifurcation diagrams. • To determine the steady-state solutions, Hopf points, and the stable and unstable zones. • To illustrate comparisons of the DDE and DPDE approaches through a selection of 2-D and 3-D solution maps. This paper studies a diffusive viral infection system with delayed immune response in the one-domain system. A system of DDE equations was explored, both analytically and numerically, using the Galerkin method. A condition that helps to find Hopf bifurcation points is determined. Full maps of the Hopf bifurcation points as well regions of stability are constructed and considered in detail. It is shown that the time delay of cytotoxic T lymphocyte (CTL) response and the diffusion parameter can significantly impact upon the stability regions. Furthermore, the influences of the other free values have been examined for their effects on stability. It is found that, as diffusion increases, the CTL response delay increases, and also as the CTL response delay is increased, the Hopf points for both generation rate and activate rate are decreased, whereas the Hopf points for the infection and death rates increased. Moreover, an increase diffusion results in an increase in the Hopf points for growth rate and activation rate, while the Hopf bifurcations are decreased for the death rate of infected cells. Bifurcation diagrams are plotted to show selected examples of limit cycle behavior (periodic oscillation), and 3-D solutions for the three concentrations in the model have been plotted to corroborate all analytical results from the theoretical section. [ABSTRACT FROM AUTHOR]

• A model for HTLV-I infection that includes uninfected & infected CD4+T cells and HTLV-I-specific CD8+T cells. • To better understand the dynamics of HTLV-I infection, we incorporate a CTL immune response delay. • Applying Lyapunov functional procedures to determine global stability by the reproduction numbers R0 and R1. • The model with delay experiences a destabilization of the infected steady state leading to Hopf bifurcation and periodic solutions. • We estimate the length of delay to preserve the stability of bifurcating limit cycle using Nyquist criteria. This paper deals with a four dimensional mathematical model for Human T-cell leukemia virus type-I (HTLV-I) infection that includes delayed CD8+ cytotoxic T-cells (CTLs) immune response. The proposed system has three biologically feasible steady states, namely disease-free steady state, CTL-inactive steady state and an interior steady state. Our theoretical analysis demonstrates that local and global stability analysis are established by the two critical parameters R 0 and R 1 , basic reproduction numbers due to viral infection and due to CTLs immune response, respectively. The disease-free steady state E 0 is globally stable if R 0 ≤ 1 , and the HTLV-I infections are eliminated. The asymptotic-carrier steady state E 1 is globally stable if R 1 ≤ 1 < R 0 , which indicates HTLV-I infection is chronic without persistence of CTLs immune response. The interior steady state E 2 is globally asymptotic stable if R 1 > 1 , which implies that the HTLV-I infection is choric in persistence of CTLs immune response. Due to immune response delay, our proposed model undergoes a destabilization of the interior steady state leading to Hopf bifurcation and periodic oscillations. We estimate the length of time delay that preserve the stability of period-1 limit cycle. We also derived the direction and stability of Hopf bifurcation around the interior steady state by center manifold theory and normal form method. To determine the robustness of the model, we performed normalized forward sensitivity analysis with reference to R 0 and R 1. Our proposed model undergoes Hopf bifurcation with respect to the production rate of uninfected CD4+T cells h , removal rate of virus-specific CTLs d 4 , spontaneous infected CD4+T cell activation d 2 and transmissibility coefficient β. Implications of our numerical illustrations to the pathogenesis of HTLV-I infection and the development of HTLV-I related HAM/TSP are explored. [ABSTRACT FROM AUTHOR]