Résumé
Relationships between the host phenotype and pathogen infection are assumed to reflect either causes or consequences of the infection. In fact, these processes are likely to co-occur, even in the same phenotypic traits. For example, hosts with high ingestion rates have a higher growth rate but are also more infected by trophically transmitted pathogens that subsequently reduce the host growth rate. Here, we briefly review the empirical evidence suggesting reciprocal effects in host-pathogen interaction. We then provide a 'verbal' model that aims to predict how reciprocal effects can bias our interpretation of the relationship between host phenotype and pathogen infection. Finally, we outline technical avenues for explicitly considering reciprocal effects in the future and discuss their fundamental and applied implications.