Abstract
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 R0 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.
Highlights
Malaria and lymphatic filariasis (LF) cause the largest public health burden of all vector-borne diseases worldwide [1] with around 350–500 million clinical episodes and 1 million deaths every year caused by malaria [2] and more than 120 million people globally infected with LF
We find that malaria prevalence is lower in humans when LF is present (Figure 5(a))
Host immunity is biased towards a Th1 response in the absence of LF, corresponding to a faster recovery from malaria and a decreased duration of infectiousness; while the presence of LF induces a greater Th2-skewed host immune response and would cause a slower Plasmodium clearance rate and increase in malaria prevalence if acting in isolation, this effect is less significant than larvalinduced mortality decreasing vector life expectancy and the time for onwards malaria transmission
Summary
Malaria and lymphatic filariasis (LF) cause the largest public health burden of all vector-borne diseases worldwide [1] with around 350–500 million clinical episodes and 1 million deaths every year caused by malaria [2] and more than 120 million people globally infected with LF. Cytokines are proteins secreted by the immune system carrying signals to cells, mediating and regulating immunity, inflammation, and the development of blood cells. They are commonly divided into two categories – type 1 and type 2. Malaria is associated with a Th1 response, with increases in the production of type 1 cytokines, including IFN-c and TNF-a [14], which stimulate immunity and can result in extreme inflammatory responses. Lymphatic filariasis induces both Th1 and Th2 responses [15,16]. Th2 levels increase, decreasing the Th1 response
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