Figure 2: A model of the host pathogen interactome illustrating how multiple gene/environment interactions might direct the attentions of the pathogen towards distinct pathways, processes, and diseases. For any pathogen, immune and pathogen defence pathways as well as inflammatory processes will be activated to counter the infection. Although the pathogen can interact with hundreds of host genes and proteins, those chosen will depend upon the strain of pathogen, the timing and localisation of infection, and on whether prior immune barriers exist. In turn, which human elements are available for interaction will depend upon their expression (time and location) upon their functional quirks dictated by polymorphisms or mutations, and so forth. This selection process, involving a genetic sieve and individual interaction probabilities, enables similar interactome selectivity, allowing the pathogen to specifically affect different series of pathways in different circumstances (illustrated by the number of human proteins ending their route in a particular pathway bin). The differential modification of particular pathways will in turn affect particular processes and endophenotypes, whose final assembly constitutes the eventual mosaic of disease. This triage, involving both human and pathogen genes and proteins, as well as environmental factors, may explain how the same pathogen could cause, prevent, or otherwise influence a variety of diseases, depending upon genetic factors and a series of coincidences (see text for further details).