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Immune subversion and quorum-sensing shape the variation in infectious dose among bacterial pathogens
João Alves Gama1, Sophie S Abby, Sara Vieira-Silva
1Centro de Biologia Ambiental and Departamento de Biologia Vegetal, Faculdade de Ciências da Universidade de Lisboa, Lisboa, Portugal.
Plos Pathogens
|February 10, 2012
Summary
Bacterial infectiousness depends on immune subversion and quorum sensing. Understanding these factors reveals how pathogens evolve, particularly emerging ones, and how small populations infect humans effectively.
Area of Science:
- Microbiology
- Evolutionary Biology
- Pathogenesis
Background:
- Pathogenic bacteria employ diverse mechanisms to infect human hosts.
- Understanding these mechanisms is crucial for studying virulence evolution from molecular and ecological viewpoints.
Purpose of the Study:
- To quantify commonalities in bacterial virulence mechanisms.
- To investigate factors associated with infectious dose 50 (ID50) in human pathogens.
Main Methods:
- Literature mining for experimental ID50 data and associated bacterial traits.
- Genome analyses to complement compiled data.
- Statistical analysis to identify correlations and explain variance in ID50.
Main Results:
- ID50 varies over 10 orders of magnitude.
- Low ID50 is linked to killing phagocytes or intracellular survival; high ID50 to motility and quorum sensing.
- Immune subversion and quorum sensing explain two-thirds of ID50 variance.
- ID50 is independent of genome size, phylogenetic inertia, secretion systems, and route of exposure.
Conclusions:
- Immune subversion is key for infection by small bacterial populations.
- Cooperative processes may aid infection by bacteria with high ID50.
- Trade-offs between growth and immune evasion shape bacterial infectiousness and virulence evolution.
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