scholarly journals Defensive Symbiosis and the Evolution of Virulence

2020 ◽  
Vol 196 (3) ◽  
pp. 333-343 ◽  
Author(s):  
Paul Nelson ◽  
Georgiana May
2018 ◽  
Author(s):  
Paul G. Nelson ◽  
Georgiana May

AbstractAlthough environments rife with enemies should cause selection for defensive traits, such enemy-rich environments should also select for greater virulence in co-occurring symbionts, yet many defensive symbionts cause little to no damage while protecting their hosts from enemies. Thus, co-infection of a defensive symbiont and a parasite is predicted to select both for increased virulence in co-infecting symbionts and for increased defense in the protective symbiont. Why then do we observe defensive mutualists that protect hosts while causing little damage? To address this question, we build a symbiont-centered model that incorporates the evolution of two independent traits: defense and virulence. Virulence is modeled as a continuous trait spanning mutualism (negative virulence) and parasitism (virulence) and thus accounts for the entire range of direct effects that symbionts have on host mortality. Defense is modeled as a continuous trait that ameliorates the costs to the host associated with co-infection with a deleterious parasite. We obtain the counterintuitive result that the evolution of increased defense in one symbiont largely leads to the evolution of lower virulence in both symbionts and may even facilitate pathogens evolving to mutualism. However, results are context-dependent and when defensive traits are costly, the evolution of greater defense may also lead to higher virulence.


2003 ◽  
Vol 71 (2) ◽  
pp. 1020-1025 ◽  
Author(s):  
Shah M. Faruque ◽  
M. Kamruzzaman ◽  
Ismail M. Meraj ◽  
Nityananda Chowdhury ◽  
G. Balakrish Nair ◽  
...  

ABSTRACT The major virulence factors of toxigenic Vibrio cholerae are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTXΦ. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of V. cholerae carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTXΦ, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the tcpA gene, 9 strains carrying a new allele of the toxT gene, and 2 strains carrying conventional tcpA and toxT genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of V. cholerae O1. Five of the 14 strains were susceptible to CTXΦ, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the tcpA and toxT genes found in environmental strains of V. cholerae encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of V. cholerae.


Parasitology ◽  
2007 ◽  
Vol 135 (3) ◽  
pp. 303-308 ◽  
Author(s):  
T. J. LITTLE ◽  
W. CHADWICK ◽  
K. WATT

SUMMARYUnderstanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for virulence.


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