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Abstract
Blood-feeding arthropods—like mosquitoes, sand flies, and ticks—transmit many diseases that impose serious public health and economic burdens. When a blood-feeding arthropod bites a mammal, it injects saliva containing immunogenic compounds that facilitate feeding. Evidence from Leishmania, Plasmodium and arboviral infections suggests that the immune responses elicited by pre-exposure to arthropod saliva can alter disease progression if the host later becomes infected. Such pre-sensitisation of host immunity has been reported to both exacerbate and limit infection symptoms, depending on the system in question, with potential implications for recovery. To explore if and how immune pre-sensitisation alters the effects of vector control, we develop a general model of vector-borne disease. We show that the abundance of pre-sensitised infected hosts should increase when control efforts moderately increase vector mortality rates. If immune pre-sensitisation leads to more rapid clearance of infection, increasing vector mortality rates may achieve greater than expected disease control. However, when immune pre-sensitisation prolongs the duration of infection, e.g., through mildly symptomatic cases for which treatment is unlikely to be sought, vector control can actually increase the total number of infected hosts. The rising infections may go unnoticed unless active surveillance methods are used to detect such sub-clinical individuals, who could provide long-lasting reservoirs for transmission and suffer long-term health consequences of those sub-clinical infections. Sensitivity analysis suggests that these negative consequences could be mitigated through integrated vector management. While the effect of saliva pre-exposure on acute symptoms is well-studied for leishmaniasis, the immunological and clinical consequences are largely uncharted for other vector-parasite-host combinations. We find a large range of plausible epidemiological outcomes, positive and negative for public health, underscoring the need to quantify how immune pre-sensitisation modulates recovery and transmission rates in vector-borne diseases.
Highlights
When a mammal is bitten by a blood feeding arthropod, it is injected with vasodilatory and immunomodulatory compounds in the arthropod’s saliva that facilitate feeding [1,2,3,4]
We modelled vector-borne disease dynamics as a set of ordinary differential equations (ODE), and alternatively, as a set of delay differential equations (DDE) that track the change in the abundance of three vector and five host classes
To examine whether our results are sensitive to the assumption of large variability in the duration of the EIP, we formulated the model as a system of delay differential equations (DDEs), which assumes the opposite extreme of no variation in EIP: all exposed vectors require exactly the length of the mean EIP, or 1/σV days to become infectious, though some vectors may not survive that period
Summary
When a mammal is bitten by a blood feeding arthropod, it is injected with vasodilatory and immunomodulatory compounds in the arthropod’s saliva that facilitate feeding [1,2,3,4]. Local immune responses to an arthropod bite include inflammation, production of anti-salivary protein antibody and recruitment of immune cells to the skin. These same arthropods can be vectors of important parasites and a recent focus of research has been elucidating the influence of salivary proteins on transmission of a wide array of diseases, including those caused by protozoan parasites such as Plasmodium and Leishmania and arboviruses such as dengue and West Nile virus [5,6,7,8,9,10]. In a majority of lab experiments, parasites that are co-inoculated with vector saliva or salivary proteins show higher infection success than when parasites are injected alone [11, 12]. Co-inoculation can benefit parasite establishment through saliva proteins that modulate host immune responses (e.g., downregulating harmful pathways or upregulating pathways that will inhibit parasite-specific responses) and can lead to the recruitment of immune cells that those parasites exploit for replication [5, 7, 8, 12]
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