Infection is a complex biological process involving reciprocally both the intensity of host exposure to a pathogen as well as the host intrinsic ''receptivity'', or permissiveness to infection. Disentangling their respective contributions is currently seen as a fundamental gap in our knowledge. Here, we take the advantage of a rare semi-natural experiment context provided by the emergence of the West Nile Virus (WNV) in North America. Focusing on the pathogen emergence period, we combine datasets from (i) wild birds exposed to WNV in an urban zoo to evaluate the species intrinsic receptivity to WNV infection in an environment where exposure to WNV vectors can be assumed to be relatively homogenous for all captive species, and (ii) from free-ranging birds in their natural habitat where species ecological traits is expected to influence their exposure to WNV vectors. We show that ecological trait and intrinsic receptivity to infection both contribute similarly to the species variation in WNV seroprevalence, but considering only one of them can lead to erroneous conclusions. We then argue that degree of pathogen host specialization could be a fundamental factor for the respective contribution of species exposure and receptivity for numerous pathogens.