The different approaches for testing host exploitation resulted in a very different rank order of the hosts, indicating the complexity of the factors involved.
This would be compatible with a form of coevolution where genetic variance of sexually reproducing hosts in combination with the complexity of host genetic architecture can prevent specific adaptation of the parasite.
Actin nucleation and bundling activities are separated in different ABD and the rate of actin polymerization is synergistic with the host Arp2/3 complex emphasizing the complexity of bacterially induced cytoskeletal modulation [ 65, 66].
In a conceptually similar manner, chaotic behavior has been observed in a model of bacteriophage-host interaction where the complexity of the system is introduced through inclusion of the time-delayed formation of consumable bacterial debris as a result of cell lysis [ 44, 45].
These genetic elements can be considered molecular parasites that have their own life cycle, only occasionally evolving functions that contribute to the fitness of the host organism, or that increase the complexity of the host in an irreversible manner, without necessarily increasing the host's fitness [ 47, 54].
This effect is very difficult, however, to predict or attribute to a specific change in the host metabolism, due to the complexity of the system.
In parasites, as consumers, a stepwise enrichment reflected by greater δ15N values is expected relative to their hosts [11], [13], [14], but due to the complexity of host-parasite interactions the isotopic niche of a parasite can vary depending upon the host-parasite system [15], [16].
A simple system is required to assess the complexity of host responses to viral infection.
These diverse observations reflect the complexity of host cell responses to Shigella invasion.
However, it is possible that different host factors are responsible for variations in colonization on day one compared to colonization persistence as measured on days 2 and 4. The additional suggestive QTLs identified in Table 1 linked to multiple traits illustrate the complexity of host genetic factors that respond to the presence of a bacterial pathogen.
