Introduction
Many of the most impactful infectious diseases that affect humans (influenza, malaria, human papillomavirus, etc.), livestock (porcine reproductive and respiratory syndrome, foot-and-mouth disease, etc.), and wildlife (anthrax, plague, etc.) have clusters in their population-genetic variability that we classify as strains. This variation in pathogen genotype is often associated with differences in phenotype, which can have profound effects on the efficacy of host immune defenses. While the human immune system is usually capable of preventing re-infection—i.e. infection with something to which it has been previously exposed—sufficient, divergent evolution among pathogen strains can reduce the ability of the host to recognize, and thus mount an immunological response to, subsequent exposures. In some cases, this change is not sufficient to completely avoid recognition by the host's immune system, yielding an immune response that is neither as strong as it would be in the case of re-exposure to the same strain, nor as weak as in the case of exposure to a novel pathogen. This partial cross-reactive immunity can likewise lead to reduced transmissibility, affecting disease dynamics across the population.