ArticleProceedings. Biological sciences2016
The emergence of latent infection in the early evolution of Mycobacterium tuberculosis.
Article in Proceedings. Biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Pan and Core Genome Analysis of 183Antibiotics (Basel, Switzerland) · 2021Article
- Integrating mathematical models with experimental data to investigate the within-host dynamics of bacterial infections.Pathogens and disease · 2019Review
- From Evolutionary Advantage to Disease Agents: Forensic Reevaluation of Host-Microbe Interactions and Pathogenicity.Microbiology spectrum · 2017Review
- Controlled fire use in early humans might have triggered the evolutionary emergence of tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis has an unusual natural history in that the vast majority of its human hosts enter a latent state that is both non-infectious and devoid of any symptoms of disease. From the pathogen perspective, it seems counterproductive to relinquish reproductive opportunities to achieve a détente with the host immune response. However, a small fraction of latent infections reactivate to the disease state. Thus, latency has been argued to provide a safe harbour for future infections which optimizes the persistence of M. tuberculosis in human populations. Yet, if a pathogen begins interactions with humans as an active disease without latency, how could it begin to evolve latency properties without incurring an immediate reproductive disadvantage? We address this question with a mathematical model. Results suggest that the emergence of tuberculosis latency may have been enabled by a mechanism akin to cryptic genetic variation in that detrimental latency properties were hidden from natural selection until their expression became evolutionarily favoured.
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