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<p>This study investigates a viral infection dynamics model that incorporates cell-to-cell transmission, latency, and a generalized humoral immune response. We rigorously establish the existence and uniqueness, boundedness, and asymptotic smoothness of the model’s semi-flow solution, discuss the local and global stability of equilibria, and identify two key thresholds (<InlineEquation ID="IEq1"> <EquationSource Format="MATHML"><math> <msub> <mi mathvariant="script">R</mi> <mn>0</mn> </msub> </math></EquationSource> <EquationSource Format="TEX">$\mathcal{R}_{0}$</EquationSource> </InlineEquation> and <InlineEquation ID="IEq2"> <EquationSource Format="MATHML"><math> <msub> <mi mathvariant="script">R</mi> <mn>1</mn> </msub> </math></EquationSource> <EquationSource Format="TEX">$\mathcal{R}_{1}$</EquationSource> </InlineEquation>) that govern the model’s global dynamics. To demonstrate that HIV transmission may indeed exhibit the described dynamic behaviours, we fit viral load data from two HIV cases, revealing distinct immune states in the two patients.</p>

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Stability analysis of age-structured viral infection dynamics with cell-to-cell transmission and humoral immunity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月11日

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  • Chenxi Ding,
  • Zhixiang Dai,
  • Xiaoqun Li,
  • Changlei Tan,
  • Nurbek Azimaqin,
  • Ruixia Yuan,
  • Yong Li

摘要

This study investigates a viral infection dynamics model that incorporates cell-to-cell transmission, latency, and a generalized humoral immune response. We rigorously establish the existence and uniqueness, boundedness, and asymptotic smoothness of the model’s semi-flow solution, discuss the local and global stability of equilibria, and identify two key thresholds ( R 0 $\mathcal{R}_{0}$ and R 1 $\mathcal{R}_{1}$ ) that govern the model’s global dynamics. To demonstrate that HIV transmission may indeed exhibit the described dynamic behaviours, we fit viral load data from two HIV cases, revealing distinct immune states in the two patients.