<p>This study investigates the spatiotemporal dynamics of HIV infection using a novel reaction-diffusion model that incorporates distributed delays, multiple transmission routes (T-V, T-I, T-C), and a cytotoxic T lymphocyte (CTL) immune response. The model improves upon previous approaches by integrating nonlinear incidence rates, spatial diffusion, and distributed delays to better capture biological realism. Analytical results establish the well-posedness of the solutions and reveal threshold dependent stability: the disease-free equilibrium <InlineEquation ID="IEq1"> <EquationSource Format="TEX">\(\mathcal{E}_0\)</EquationSource> </InlineEquation> is globally stable when the basic reproduction number <InlineEquation ID="IEq2"> <EquationSource Format="TEX">\(\mathfrak{R}_0 &lt; 1\)</EquationSource> </InlineEquation>; the immune-free equilibrium <InlineEquation ID="IEq3"> <EquationSource Format="TEX">\(\mathcal{E}_1\)</EquationSource> </InlineEquation> is globally stable when <InlineEquation ID="IEq4"> <EquationSource Format="TEX">\(\mathfrak{R}_0 &gt; 1 &gt; \mathfrak{R}_{CTL}\)</EquationSource> </InlineEquation>; the infected equilibrium <InlineEquation ID="IEq5"> <EquationSource Format="TEX">\(\mathcal{E}_2\)</EquationSource> </InlineEquation>, which involves an active CTL response, is globally stable when <InlineEquation ID="IEq6"> <EquationSource Format="TEX">\(\mathfrak{R}_{CTL} &gt; 1\)</EquationSource> </InlineEquation>. Numerical simulations validate the analytical findings and demonstrate the model’s ability to represent complex HIV dynamics. This work provides a robust theoretical framework for understanding HIV progression and immune control, with potential implications for the design of therapeutic strategies.</p>

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Dynamical analysis of an infectious disease model with diffusion, distributed delays and multiple transmission routes

  • Chong Chen,
  • Zhijian Ye,
  • Yinggao Zhou

摘要

This study investigates the spatiotemporal dynamics of HIV infection using a novel reaction-diffusion model that incorporates distributed delays, multiple transmission routes (T-V, T-I, T-C), and a cytotoxic T lymphocyte (CTL) immune response. The model improves upon previous approaches by integrating nonlinear incidence rates, spatial diffusion, and distributed delays to better capture biological realism. Analytical results establish the well-posedness of the solutions and reveal threshold dependent stability: the disease-free equilibrium \(\mathcal{E}_0\) is globally stable when the basic reproduction number \(\mathfrak{R}_0 < 1\) ; the immune-free equilibrium \(\mathcal{E}_1\) is globally stable when \(\mathfrak{R}_0 > 1 > \mathfrak{R}_{CTL}\) ; the infected equilibrium \(\mathcal{E}_2\) , which involves an active CTL response, is globally stable when \(\mathfrak{R}_{CTL} > 1\) . Numerical simulations validate the analytical findings and demonstrate the model’s ability to represent complex HIV dynamics. This work provides a robust theoretical framework for understanding HIV progression and immune control, with potential implications for the design of therapeutic strategies.