Ponente
Descripción
Understanding the within-host dynamics of viral infections is fundamental for elucidating disease progression and improving therapeutic strategies. This work presents a system of ordinary differential equations that describes the interactions among susceptible and infected respiratory epithelial cells, free viral particles, and the adaptive immune response mediated by T-helper ($T_h$) lymphocytes. The model aims to investigate how $T_h$ lymphocyte activation influences viral control and the progression of infection.
A qualitative analysis is performed by deriving a modified basic reproduction number, $R_0^*$, which explicitly incorporates the effect of $T_h$ lymphocyte activation. The analysis shows that $R_0^*$ is lower than the classical basic reproduction number obtained in the absence of an adaptive immune response, indicating that $T_h$-mediated immunity reduces the threshold for viral establishment. The stability analysis identifies three biologically relevant equilibrium states: a disease-free equilibrium, an infected equilibrium without $T_h$ cell activation, and an endemic equilibrium characterized by an active adaptive immune response.
Numerical simulations, illustrate the temporal dynamics of the infection and demonstrate that increasing viral load promotes $T_h$ lymphocyte activation and cytokine production, enhancing the elimination of infected cells and accelerating viral clearance. In contrast, depletion of $T_h$ lymphocytes delays viral elimination despite increased phagocytic activity, underscoring the essential role of adaptive immunity in controlling infection. These findings provide a quantitative framework for understanding immune-virus interactions and offer a useful tool for evaluating immune dysfunction, therapeutic interventions, and the potential effects of viral evolution.