Abstract
Analysis of 15 serovars of Chlamydia trachomatis reveals an evolutionary arms race in pathogen-host interactions.
Highlights
The genomes of pathogens are thought to have evolved under selective pressure provided by the host in a coevolutionary arms race
On behalf of the arms race theory assumed by the evolutionary Red Queen's Hypothesis [15,16], one question arises: do distinct host organs differently shape the genome of the same pathogen? No microrganism is more suitable than Chlamydia trachomatis, the most prevalent sexually transmitted bacterial pathogen worldwide, to test this hypothesis, as the species comprises several serovars with a wide range of specific human tissue tropism
This pathogen is mainly classified into 15 serovars based on the differential immunoreactivity of the major outer membrane protein (MOMP), constituting three disease groups [17]: serovars A-C and Ba are commonly associated with ocular trachoma; serovars D-K infect the epithelial cells of genitalia and are normally found in non-invasive sexually transmitted infections; serovars L1-L3 are sexually transmitted but are invasive and disseminate into the local lymph nodes causing lymphogranuloma venereum (LGV)
Summary
The genomes of pathogens are thought to have evolved under selective pressure provided by the host in a coevolutionary arms race (the 'Red Queen's Hypothesis'). Adaptation by pathogens is thought to rely not on whole chromosome dynamics but on gain/loss of specific genes, yielding differential abilities to infect distinct tissues It is not known whether distinct host organs differently shape the genome of the same pathogen. An extreme example is provided by the well-studied E. coli, where strains K-12 and O157 differ by more than 1 million base pairs [12], and same-serovar strains were found to present profound differences in gene content [13,14] These targeted HGT events reflect different pathoadaptation processes for microrganisms with reversible genome size-plasticity; depending on the transitory 'cassette-genes' carried at any specific time, the pathogenecity or ability of these microrganisms to infect different tissues may vary [7]. In the context of this classification system, the evaluation of adaptive evolution becomes enigmatic because there is no correlation between it and C. trachomatis tropism nor with the ecological success of the different serovars, as strains with different organ specificities are placed within the same classification group
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