By breaking the environment into host and guest operating systems, the hypervisor can be more secure.
For this reason, methods to break this tolerance, such as presenting the critical epitope in a different molecular environment to the tolerised host, have been developed.
Indeed, this type of management frequently leads to break the balance between pathogen and host, consequently resulting in the emergence of infectious and parasitic diseases which cause various problems ranging from slow up growth, reduced fertility rates, until the appearance of severe epidemics resulting in high mortality (Scholz 1999).
There is growing awareness that drivers of disease emergence modulate the interplay between pathogens, hosts and environment.
Furthermore, the pathogenic genes are generally differentially expressed before and after the pathogen invading its host so that the pathogen can successfully break through its host immune system and adopt its life inside the host.
This may also be due to particular mechanisms that cannot be easily broken down by pathogens.
This new information extend our understanding in the pathogen-host cell interactions, host cellular responses, disease pathogenesis, host immune responses, and eventually new therapeutics and novel vaccine development.
During the dynamically changing environment of host-pathogen interactions, both host and pathogen have evolved numerous strategies for adaptation.
Future research should be conducted to explore the virulence components of all six pathogens identified in this study and to test the contribution of multiple factors (pathogen, environment and host related) to the aetiology of WS.
Pathogen-host interactions during bacterial infection expose bacteria to multiple physiological and biological stresses, and intracellular pathogens are known to adapt to changes in their environment, avoiding degradation by host cell defense systems by coordinated regulation of gene expression.
