Immuno-epidemiology: closing the immunity-transmission cycle
Individual hosts differ considerably in the way in which they respond to the same pathogen. This is not only caused by genetic polymorphism determining immune reaction (e.g. MHC), but also by the infection history of the individual (e.g. influenza, parasites with acquired immunity, dengue). An individual's history is a result of the past pattern of transmission in the population. Population transmission (infection pressure) by itself is the collective output of infectious material by the individuals that constitute the population, which in turn is decided by each individual's reaction to the pathogen. This closes a circle of mutual interaction and influence. This cycle influences the population effects of control measures aimed at individuals, and the evolution of resistance and virulence. In order to understand these processes we need a fuller understanding of the immunity-transmission cycle.
Presently immunological theory and epidemiological theory restrict themselves to one part of the cycle, both making 'black box', or rudimentary and idealized, assumptions about the other half (when the influence of this half is considered at all). Almost never is there full feedback between the within- and between-host processes. For the understanding of the evolution of resistance and virulence, however, one has to close the loop. Variants of the infectious agent arise within individuals, but will only be relevant at the population level if they also spread between individuals. One currently lacks the tools to make even qualitative predictions, for example for the population consequences of vaccination when there is great polymorphism in an individual's immune reaction (through genetic polymorphism and/or due to previous memory/exposure). Obvious examples are malaria and dengue.
It is our aim in this 2½-day workshop to bring together experts on several parts of the immunity-transmission cycle where we want to take, in a structured way, a necessary step towards integration. The central theme is to develop sensible and simple within-host immunological models that can be merged in sensible and simple between-host epidemiological models, and to explore the full cycle and its effects on pathogen evolution, spread and control. Issues to be addressed involve cellular versus humoral immunity, short-lived versus long-lived memory, acquired immunity, polymorphism, evolution of resistance and virulence.
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