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the optimal controls introduced in our mathematical model respond automatically to the epidemic once it is detected, and there is an analogy between their shapes and the shape of infection.
As a first analysis of the potential effect of the shape of infection duration distribution on global dynamics, all intra-population parameters have been considered consistent among populations of the network.
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The values of the optimal controls are small but realize our main objective presented in (7), but the most important idea we can extract from the results in both Figures 20 and 21 is that there is an analogy between shapes of infection and optimal control functions since whenever the infection is maximal, the optimal controls which are associated with it become simultaneously maximal.
The epidemiology of schistosome infection in this population followed a convex shape of rising infection levels (intensity and prevalence) peaking in childhood and declining with age thereafter, a pattern which has been attributed to cumulative exposure to infection and the development of gradually acquired resistance to schistosomes [ 8, 11, 14, 20, 42].
As already mentioned above, in the metapopulation framework, we were not exclusively interested in the potential effect of the shape of the infection duration distribution on epidemic dynamics.
The importance of this finding is that any acquired immunity developed by the host to B. pseudomallei [ 24] is unlikely to be significant enough to shape the epidemiology of infection in endemic populations.
The goals of such studies were detailed analyses of dietary, medicinal, and environmental factors that shaped the patterns of infection.
These observations support the notion that stochasticity is an important factor shaping the outcome of infection.
The same method was used as one of the techniques of shaping the force of infection of HIV in the Estimation and Projection Package (EPP) estimation approach [ 7].
Compared to (v), (vii) has the advantage that assumptions about the full shape of the force of infection function are unnecessary.
Some anti-bacterial defence mechanisms, operating at a subnormal level during all stages of RA, result in an RA-predisposing exposure to microbial antigens in the shape of commensals and infections.
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