How infection-triggered pathobionts influence virulence evolution

Franz, Mathias; Regoes, Roland R.; Rolff, Jens

doi:10.1098/rstb.2023.0067

Cited by 2 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a result, the receptor and signalling stages lack the specificity needed to mount gene induction precise enough to be useful only against the pathogen that initiated the response—coinfections are likely in natural settings anyways (see discussion by Franz et al . [ 1 ]). Consequently, there is little benefit to precision at the recognition and signalling stage.…”

Section: Information Bottlenecks Lead To Generalist Immune Activationmentioning

confidence: 99%

When the microbiome shapes the host: immune evolution implications for infectious disease

Hanson

2024

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

The microbiome includes both ‘mutualist’ and ‘pathogen’ microbes, regulated by the same innate immune architecture. A major question has therefore been: how do hosts prevent pathogenic infections while maintaining beneficial microbes? One idea suggests hosts can selectively activate innate immunity upon pathogenic infection, but not mutualist colonization. Another idea posits that hosts can selectively attack pathogens, but not mutualists. Here I review evolutionary principles of microbe recognition and immune activation, and reflect on newly observed immune effector–microbe specificity perhaps supporting the latter idea. Recent work in Drosophila has found a surprising importance for single antimicrobial peptides in combatting specific ecologically relevant microbes. The developing picture suggests these effectors have evolved for this purpose. Other defence responses like reactive oxygen species bursts can also be uniquely effective against specific microbes. Signals in other model systems including nematodes, Hydra , oysters, and mammals, suggest that effector–microbe specificity may be a fundamental principle of host–pathogen interactions. I propose this effector–microbe specificity stems from weaknesses of the microbes themselves: if microbes have intrinsic weaknesses, hosts can evolve effectors that exploit those weaknesses. I define this host–microbe relationship as ‘the Achilles principle of immune evolution’. Incorporating this view helps interpret why some host–microbe interactions develop in a coevolutionary framework (e.g. Red Queen dynamics), or as a one-sided evolutionary response. This clarification should be valuable to better understand the principles behind host susceptibilities to infectious diseases. This article is part of the theme issue ‘Sculpting the microbiome: how host factors determine and respond to microbial colonization’.

show abstract

Section: Information Bottlenecks Lead To Generalist Immune Activationmentioning

confidence: 99%

When the microbiome shapes the host: immune evolution implications for infectious disease

Hanson

2024

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

show abstract

“…Franz et al . [ 16 ] provide a unique perspective of how microbe-microbe interactions play out in the host given different infectious states. Their modelling study provides a basis for the evolutionary trajectories of the virulence of pathobionts, commensal microbes that can act in a virulent fashion upon disruption of host homeostasis.…”

Section: Summary Of Articlesmentioning

confidence: 99%

“…Franz et al . [ 16 ] explore the biologically realistic and woefully under-studied situation of co-infection, asking how the virulence of the initiating pathogen, the pathobiont and the overall system is shaped by different parameters of the infectious process.…”

Section: Summary Of Articlesmentioning

confidence: 99%