DIFFERENT LIFE-STYLES OF HUMAN PATHOGENIC PROKARYOTES AND THEIR STRATEGIES FOR PHASE AND ANTIGENIC VARIATION

Authors
Citation
M. Fussenegger, DIFFERENT LIFE-STYLES OF HUMAN PATHOGENIC PROKARYOTES AND THEIR STRATEGIES FOR PHASE AND ANTIGENIC VARIATION, Symbiosis, 22(1-2), 1997, pp. 85-153
Citations number
339
Categorie Soggetti
Microbiology
Journal title
ISSN journal
03345114
Volume
22
Issue
1-2
Year of publication
1997
Pages
85 - 153
Database
ISI
SICI code
0334-5114(1997)22:1-2<85:DLOHPP>2.0.ZU;2-H
Abstract
Bacteria generally cause disease in a mammalian host by a multifacette d process involving numerous components, each one of which may be nece ssary for pathogenesis. These virulence determinants include a variety of factors that enable colonization of a specific niche in the host, evasion of host immune responses, invasion of mammalian tissues and/or cells, or direct host toxicity. The mechanisms used by pathogenic bac teria to cause infection and disease are diverse, but they usually inc lude a co-regulated group of complementary genetic properties that are best suited for the interaction of a particular microorganism with a particular host. However, because of their need to overcome similar ho st and environmental barriers, common themes of microbial pathogenesis have evolved in quite distinct bacterial species. We describe here fo ur different but rather general strategies of host-pathogen interactio ns and outline the crosstalks which take place at the molecular level during different stages of an infection. Because they deal with variou s microenvironments during the course of infection, most bacterial pat hogens evolved different mechanisms for generating genetic variation. The ability to vary their cell-surface composition may often play a ke y role in the evasion of antigen-specific host immune defences. In add ition, it may promote expression of the most appropriate cell-surface structures for a given microenvironment or infection stage, thereby op timizing the virulence potential of a bacterial pathogen during the co urse of infection. Here we review, in the context of the corresponding infection processes, mechanisms that bring about this antigenic and p hase variation as well as its functional consequences.