Research article

Immuno-epidemiological co-affection model of HIV infection and opioid addiction


  • Received: 10 November 2021 Revised: 12 January 2022 Accepted: 17 January 2022 Published: 08 February 2022
  • In this paper, we present a multi-scale co-affection model of HIV infection and opioid addiction. The population scale epidemiological model is linked to the within-host model which describes the HIV and opioid dynamics in a co-affected individual. CD4 cells and viral load data obtained from morphine addicted SIV-infected monkeys are used to validate the within-host model. AIDS diagnoses, HIV death and opioid mortality data are used to fit the between-host model. When the rates of viral clearance and morphine uptake are fixed, the within-host model is structurally identifiable. If in addition the morphine saturation and clearance rates are also fixed the model becomes practical identifiable. Analytical results of the multi-scale model suggest that in addition to the disease-addiction-free equilibrium, there is a unique HIV-only and opioid-only equilibrium. Each of the boundary equilibria is stable if the invasion number of the other epidemic is below one. Elasticity analysis suggests that the most sensitive number is the invasion number of opioid epidemic with respect to the parameter of enhancement of HIV infection of opioid-affected individual. We conclude that the most effective control strategy is to prevent opioid addicted individuals from getting HIV, and to treat the opioid addiction directly and independently from HIV.

    Citation: Churni Gupta, Necibe Tuncer, Maia Martcheva. Immuno-epidemiological co-affection model of HIV infection and opioid addiction[J]. Mathematical Biosciences and Engineering, 2022, 19(4): 3636-3672. doi: 10.3934/mbe.2022168

    Related Papers:

  • In this paper, we present a multi-scale co-affection model of HIV infection and opioid addiction. The population scale epidemiological model is linked to the within-host model which describes the HIV and opioid dynamics in a co-affected individual. CD4 cells and viral load data obtained from morphine addicted SIV-infected monkeys are used to validate the within-host model. AIDS diagnoses, HIV death and opioid mortality data are used to fit the between-host model. When the rates of viral clearance and morphine uptake are fixed, the within-host model is structurally identifiable. If in addition the morphine saturation and clearance rates are also fixed the model becomes practical identifiable. Analytical results of the multi-scale model suggest that in addition to the disease-addiction-free equilibrium, there is a unique HIV-only and opioid-only equilibrium. Each of the boundary equilibria is stable if the invasion number of the other epidemic is below one. Elasticity analysis suggests that the most sensitive number is the invasion number of opioid epidemic with respect to the parameter of enhancement of HIV infection of opioid-affected individual. We conclude that the most effective control strategy is to prevent opioid addicted individuals from getting HIV, and to treat the opioid addiction directly and independently from HIV.



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