21 research outputs found

    Human LF prevalence as a function of worm death rate in malaria-infected hosts.

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    <p>Considerable differences in LF prevalence are observed when malaria is introduced to the system depending on mean worm life expectancy.</p

    Invasion of (a and b) malaria in LF endemic regions, and (c and d) LF in malaria endemic regions.

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    <p>Prevalence time-series, in hosts and vectors, when introducing malaria or LF into endemic regions of the other.</p

    Basic structure of the malaria model.

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    <p>See <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1003096#pcbi-1003096-t001" target="_blank">Tables 1</a> and <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1003096#pcbi-1003096-t002" target="_blank">2</a> for a summary of state variables and parameters.</p

    State variables in the full co-infection model (where and ).

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    <p>State variables in the full co-infection model (where and ).</p

    Modelling Co-Infection with Malaria and Lymphatic Filariasis

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    <div><p>Malaria and lymphatic filariasis (LF) continue to cause a considerable public health burden globally and are co-endemic in many regions of sub-Saharan Africa. These infections are transmitted by the same mosquito species which raises important questions about optimal vector control strategies in co-endemic regions, as well as the effect of the presence of each infection on endemicity of the other; there is currently little consensus on the latter. The need for comprehensive modelling studies to address such questions is therefore significant, yet very few have been undertaken to date despite the recognised explanatory power of reliable dynamic mathematical models. Here, we develop a malaria-LF co-infection modelling framework that accounts for two key interactions between these infections, namely the increase in vector mortality as LF mosquito prevalence increases and the antagonistic Th1/Th2 immune response that occurs in co-infected hosts. We consider the crucial interplay between these interactions on the resulting endemic prevalence when introducing each infection in regions where the other is already endemic (e.g. due to regional environmental change), and the associated timescale for such changes, as well as effects on the basic reproduction number <i>R<sub>0</sub></i> of each disease. We also highlight potential perverse effects of vector controls on human infection prevalence in co-endemic regions, noting that understanding such effects is critical in designing optimal integrated control programmes. Hence, as well as highlighting where better data are required to more reliably address such questions, we provide an important framework that will form the basis of future scenario analysis tools used to plan and inform policy decisions on intervention measures in different transmission settings.</p></div

    Malaria and LF prevalence in (a) humans and (b) mosquitoes with and without co-infection.

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    <p>Malaria and LF are introduced simultaneously into a population in the presence and absence of co-infection (with <i>a</i>β€Š=β€Š0.2 day<sup>βˆ’1</sup>).</p

    Dependence of <i>R<sub>0</sub><sup>M</sup></i> on LF prevalence in hosts for different mosquito biting rates.

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    <p>Dependence of <i>R<sub>0</sub><sup>M</sup></i> on LF prevalence in hosts for different mosquito biting rates.</p

    Worm mortality rate and malaria recovery rate as functions of mean worm burden.

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    <p>Increases in worm burden skew the immune system towards a Th2 response, lowering worm mortality rate (a) and human recovery rate (b) from malaria. The two curves in (a) represent the worm death rate in malaria-infected (upper) and malaria-susceptible human hosts (lower).</p

    Structure of the full malaria-LF co-infection model.

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    <p>(NB. Life stage transition arrows from each <i>L</i> compartment to each <i>W</i> compartment should also strictly be present, but these are omitted here for clarity. All birth and deaths rates are also omitted, as well as the labelling of rates in terms of model parameters).</p

    Basic structure of the LF model.

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    <p>See <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1003096#pcbi-1003096-t001" target="_blank">Tables 1</a> and <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1003096#pcbi-1003096-t002" target="_blank">2</a> for a summary of state variables and parameters.</p
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