Historically, pathogenesis research has focused on the identification and characterization of virulence factors. More recently, 'anti-virulence' genes have been discovered. Mutations in these loci result in a hypervirulent phenotype, as measured by a lower lethal dose, a colonization advantage, reduced clearance or decreased survival time of the host. If these genes function to reduce pathogen virulence, why have they been retained? Multiple hypotheses have been offered to explain this phenomenon.