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On latencies in malaria infections and their impact on the disease dynamics

  • Received: 01 February 2012 Accepted: 29 June 2018 Published: 01 January 2013
  • MSC : Primary: 92D25, 92D30; Secondary: 37G99.

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    In this paper, we modify the classic Ross-Macdonald model for malaria disease dynamics by incorporating latencies both for human beings and female mosquitoes. One novelty of our model is that we introduce two general probability functions ($P_1(t)$ and $P_2(t)$) to reflect the fact that the latencies differ from individuals to individuals. We justify the well-posedness of the new model, identify the basic reproduction number $\mathcal{R}_0$ for the model and analyze the dynamics of the model. We show that when $\mathcal{R}_0 <1 the="" disease="" free="" equilibrium="" e_0="" is="" globally="" asymptotically="" stable="" meaning="" that="" the="" malaria="" disease="" will="" eventually="" die="" out="" and="" if="" mathcal="" r="" _0="">1$, $E_0$ becomes unstable.When $\mathcal{R}_0 >1$, we consider two specific forms for $P_1(t)$ and $P_2(t)$: (i) $P_1(t)$ and $P_2(t)$ are both exponential functions; (ii) $P_1(t)$ and $P_2(t)$ are both step functions.For (i), the model reduces to an ODE system, and for (ii), the long term disease dynamics are governed by a DDE system. In both cases, we are able to show that when $\mathcal{R}_0>1$ then the disease will persist; moreover if there is no recovery ($\gamma_1=0$), then all admissible positive solutions will converge to the unique endemic equilibrium. A significant impact of the latencies is that they reduce the basic reproduction number, regardless of the forms of the distributions.

    Citation: Yanyu Xiao, Xingfu Zou. On latencies in malaria infections and their impact on the disease dynamics[J]. Mathematical Biosciences and Engineering, 2013, 10(2): 463-481. doi: 10.3934/mbe.2013.10.463

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  • In this paper, we modify the classic Ross-Macdonald model for malaria disease dynamics by incorporating latencies both for human beings and female mosquitoes. One novelty of our model is that we introduce two general probability functions ($P_1(t)$ and $P_2(t)$) to reflect the fact that the latencies differ from individuals to individuals. We justify the well-posedness of the new model, identify the basic reproduction number $\mathcal{R}_0$ for the model and analyze the dynamics of the model. We show that when $\mathcal{R}_0 <1 the="" disease="" free="" equilibrium="" e_0="" is="" globally="" asymptotically="" stable="" meaning="" that="" the="" malaria="" disease="" will="" eventually="" die="" out="" and="" if="" mathcal="" r="" _0="">1$, $E_0$ becomes unstable.When $\mathcal{R}_0 >1$, we consider two specific forms for $P_1(t)$ and $P_2(t)$: (i) $P_1(t)$ and $P_2(t)$ are both exponential functions; (ii) $P_1(t)$ and $P_2(t)$ are both step functions.For (i), the model reduces to an ODE system, and for (ii), the long term disease dynamics are governed by a DDE system. In both cases, we are able to show that when $\mathcal{R}_0>1$ then the disease will persist; moreover if there is no recovery ($\gamma_1=0$), then all admissible positive solutions will converge to the unique endemic equilibrium. A significant impact of the latencies is that they reduce the basic reproduction number, regardless of the forms of the distributions.


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