Narrow Results

In this work, we propose and investigate a human immunodeficiency virus (HIV) infection model that considers CD4${}^{+}$ T cell homeostasis and the cytotoxic T lymphocyte (CTL) response. The local stability of the disease-free and endemic equilibrium point is established. Further, the global stability of the disease-free and endemic equilibrium points is investigated. Under specific parametric conditions, it is shown that the model exhibits backward, forward (transcritical) bifurcation, Hopf and Hopf–Hopf bifurcation. We have further considered a time lag in the model to represent the time delay between CD4${}^{+}$ T cell infection and the viral particle production and performed the stability and bifurcation analysis for the delay model. We conduct comprehensive numerical experiments to visualize the dynamical behavior of the HIV model and validate our findings.

Quasiperiodicity and chaos in a ring of unidirectionally coupled sigmoidal neurons (a ring neural oscillator) caused by a single shortcut is examined. A codimension-two Hopf–Hopf bifurcation for two periodic solutions exists in a ring of six neurons without self-couplings and in a ring of four neurons with self-couplings in the presence of a shortcut at specific locations. The locus of the Neimark–Sacker bifurcation of the periodic solution emanates from the Hopf–Hopf bifurcation point and a stable quasiperiodic solution is generated. Arnold’s tongues emanate from the locus of the Neimark–Sacker bifurcation, and multiple chaotic oscillations are generated through period-doubling cascades of periodic solutions in the Arnold’s tongues. Further, such chaotic irregular oscillations due to a single shortcut are also observed in propagating oscillations in a ring of Bonhoeffer–van der Pol (BVP) neurons coupled unidirectionally by slow synapses.

This paper is concerned with the effect of predator cannibalism in a delayed diffusive predator–prey system. We aim for the case where the corresponding linear system has two pairs of purely imaginary eigenvalues at a critical point, leading to Hopf–Hopf bifurcation. An approach of center manifold reduction is applied to derive the normal form for such nonresonant Hopf–Hopf bifurcations. We find that the system exhibits very rich dynamics, including the coexistence of periodic and quasi-periodic oscillations. Numerically, we show that Hopf–Hopf bifurcation is induced if the strength of the predator cannibalism term belongs to an appropriate interval.

The dynamics of a delay Sel’kov–Schnakenberg reaction–diffusion system are explored. The existence and the occurrence conditions of the Turing and the Hopf bifurcations of the system are found by taking the diffusion coefficient and the time delay as the bifurcation parameters. Based on that, the existence of codimension-2 bifurcations including Turing–Turing, Hopf–Hopf and Turing–Hopf bifurcations are given. Using the center manifold theory and the normal form method, the universal unfolding of the Turing–Hopf bifurcation at the positive constant steady-state is demonstrated. According to the universal unfolding, a Turing–Hopf bifurcation diagram is shown under a set of specific parameters. Furthermore, in different parameter regions, we find the existence of the spatially inhomogeneous steady-state, the spatially homogeneous and inhomogeneous periodic solutions. Discretization of time and space visualizes these spatio-temporal solutions. In particular, near the critical point of Hopf–Hopf bifurcation, the spatially homogeneous periodic and inhomogeneous quasi-periodic solutions are found numerically.

During disease outbreak, it has been observed that information about the disease prevalence induces the individual’s behavioral changes. This information is usually assumed to be generated by the density of infective individuals and active mass media. The delay in reporting of these infective individuals may have its impact on generated information. Hence, to study the impact of delay on information generation, and therefore on the disease dynamics, a delay differential equation model is proposed and analyzed. The dynamics of information with delay effect is also modeled by a separate rate equation. Model analysis is performed and a unique infected equilibrium is obtained when the basic reproduction number ($R_0$) is greater than one, whereas the disease free equilibrium always exists. When $R_0<1$, the disease free equilibrium is found to be locally stable independent of delay effect. The unique infected equilibrium is found to be locally stable till delay reaches a threshold value. The global stability of the unique infected equilibrium is also established under some parametric conditions by constructing a suitable Lyapunov function. The occurrence of Hopf bifurcation is observed when the delay in information crosses the threshold value. Analytically, the direction and stability of bifurcating periodic solutions is established. Further, we observed the occurrence of Hopf-Hopf bifurcation at two different delays. At first delay threshold, the endemic equilibrium loses its stability and produces periodic oscillations via Hopf bifurcation. It further regains its stability at second delay threshold via another Hopf bifurcation. Hence, the delay effect on information shows possibility of stability switches. Numerical experiments are carried out to support the obtained analytical results. Our study infers that the disease will show persistent oscillations if there is a significant time lag in reporting of infective after the disease outbreak. Thus, the delay in dissemination of information shows rich and complex dynamics in the model and provides important insights. We also observe numerically that the saturation in information plays a significant role on stability of infected equilibrium in presence of delay.