Models for the evolution of virulence traditionally assume a trade-off between the inverse of disease-induced mortality rate and infectivity, resulting in intermediate virulence. The underlying intuition is that faster growing agent populations do both more damage and produce more infective particles. This intuition implicitly assumes a well-mixed host body. In reality both damage and infectivity depend mainly on the location in the body where the agents lodge. This is related i.a. to the surface proteins that allow agents to dock on and penetrate into different cell types. The typical example is respiratory diseases where more deeply seated ones are both less infective and more harmful. With the other standard assumption, full cross-immunity between disease strains, this would lead to evolution towards the tip of the nose. In reality cross-immunity depends on surface antigens and hence is at least in part connected to depth. In this talk I discuss a simple adaptive dynamics style model taking on board the aforementioned considerations. Inferences are that in respiratory diseases (1) higher host population densities are conducive to a higher diversity, (2) diversity should be higher in the upper air passages than lower in the lungs, (3) emerging diseases may be expected to combine a high virulence with a low infectivity.