If FPV is not a confounding factor, we cannot exclude the existence of another one, such as a greater susceptibility of certain individuals to infections whatever the parasite involved. Numerous studies have shown that an extensive inter-individual variability exists in response to certain pathogens, such as HIV (review in [100] ), trypanosomiasis (review in [101] ), or human and bovine tuberculosis (reviews in [102, 103] ), including variations in susceptibility to the parasite, its transmission, and/or the course of disease progression. It has been attributed to host determinants and variability in multiple genes that regulate virus cell entry, acquired and innate immunity (e.g., macrophages, molecular and cellular actors of the inflammatory reaction), and others that influence the outcome of the infection. Hosts with a diminished or delayed innate immune response may in fact be more susceptible to any infection, with physiological parameters, such as hormonal profiles (e.g., [104] ), possibly playing a role in the modulation of transmission efficiency and/or in the immune response intensity. A weaker physical condition could also lead to a higher sensitivity to infectious agents (lower dose-effect, different intra-host dynamic) (e.g., [105] ). More generally, individuals' personality may as well be involved [61, 106] . A better understanding of genetic, physiological and immunological basis of such inter-individual variability would therefore be of particular interest in the context of polyparasitism. Another perspective of this work is the development of new methods able to distinguish pairwise interactions from those due to common confounding factors shared by the three viruses. Such methods could use the proportion of infected individuals that are in reality triply infected.