<p>This paper presents a tuberculosis transmission model incorporating age structure and dual time delays to examine the joint effects of environmental pathways and infection-stage heterogeneity. Theoretical analysis establishes threshold dynamics dominated by the basic reproduction number <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>, demonstrating that when <InlineEquation ID="IEq2"> <EquationSource Format="MATHML"><math> <msub> <mi mathvariant="script">R</mi> <mn>0</mn> </msub> <mo>&lt;</mo> <mn>1</mn> </math></EquationSource> <EquationSource Format="TEX">$\mathcal{R}_{0}&lt;1$</EquationSource> </InlineEquation>, the system is globally asymptotically stable at the disease-free equilibrium <InlineEquation ID="IEq3"> <EquationSource Format="MATHML"><math> <msub> <mi>E</mi> <mn>0</mn> </msub> </math></EquationSource> <EquationSource Format="TEX">$E_{0}$</EquationSource> </InlineEquation> regardless of variations in <InlineEquation ID="IEq4"> <EquationSource Format="MATHML"><math> <msub> <mi>τ</mi> <mn>1</mn> </msub> </math></EquationSource> <EquationSource Format="TEX">$\tau _{1}$</EquationSource> </InlineEquation> and <InlineEquation ID="IEq5"> <EquationSource Format="MATHML"><math> <msub> <mi>τ</mi> <mn>2</mn> </msub> </math></EquationSource> <EquationSource Format="TEX">$\tau _{2}$</EquationSource> </InlineEquation>. When <InlineEquation ID="IEq6"> <EquationSource Format="MATHML"><math> <msub> <mi mathvariant="script">R</mi> <mn>0</mn> </msub> <mo>&gt;</mo> <mn>1</mn> </math></EquationSource> <EquationSource Format="TEX">$\mathcal{R}_{0}&gt;1$</EquationSource> </InlineEquation>, the system is globally asymptotically stable at the endemic equilibrium <InlineEquation ID="IEq7"> <EquationSource Format="MATHML"><math> <msub> <mi>E</mi> <mo>∗</mo> </msub> </math></EquationSource> <EquationSource Format="TEX">$E_{*}$</EquationSource> </InlineEquation> under conditions where <InlineEquation ID="IEq8"> <EquationSource Format="MATHML"><math> <msub> <mi>τ</mi> <mn>1</mn> </msub> <mo>=</mo> <msub> <mi>τ</mi> <mn>2</mn> </msub> <mo>=</mo> <mn>0</mn> </math></EquationSource> <EquationSource Format="TEX">$\tau _{1}=\tau _{2}=0$</EquationSource> </InlineEquation> or <InlineEquation ID="IEq9"> <EquationSource Format="MATHML"><math> <msub> <mi>τ</mi> <mn>1</mn> </msub> <mo>=</mo> <msub> <mi>τ</mi> <mn>2</mn> </msub> <mo>=</mo> <mi>τ</mi> <mo>&gt;</mo> <mn>0</mn> </math></EquationSource> <EquationSource Format="TEX">$\tau _{1}=\tau _{2}=\tau &gt;0$</EquationSource> </InlineEquation>. Numerical simulations not only validate these global stability conclusions but also reveal the differential regulatory effects of dual time delays. This study clarifies the regulatory mechanism of dual age-dependent infection delays on tuberculosis transmission, providing a dynamical basis for formulating relevant prevention and control strategies.</p>

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The impact of age and environment on tuberculosis transmission

  • Jiale Fan,
  • Hui Cao,
  • Danfeng Pang

摘要

This paper presents a tuberculosis transmission model incorporating age structure and dual time delays to examine the joint effects of environmental pathways and infection-stage heterogeneity. Theoretical analysis establishes threshold dynamics dominated by the basic reproduction number R 0 $\mathcal{R}_{0}$ , demonstrating that when R 0 < 1 $\mathcal{R}_{0}<1$ , the system is globally asymptotically stable at the disease-free equilibrium E 0 $E_{0}$ regardless of variations in τ 1 $\tau _{1}$ and τ 2 $\tau _{2}$ . When R 0 > 1 $\mathcal{R}_{0}>1$ , the system is globally asymptotically stable at the endemic equilibrium E $E_{*}$ under conditions where τ 1 = τ 2 = 0 $\tau _{1}=\tau _{2}=0$ or τ 1 = τ 2 = τ > 0 $\tau _{1}=\tau _{2}=\tau >0$ . Numerical simulations not only validate these global stability conclusions but also reveal the differential regulatory effects of dual time delays. This study clarifies the regulatory mechanism of dual age-dependent infection delays on tuberculosis transmission, providing a dynamical basis for formulating relevant prevention and control strategies.