Scientists have produced a new analysis of dozens of tuberculosis genomes gathered from around the world, from this researchers have produced a more detailed picture of why tuberculosis (TB) is so prevalent and how it evolves to resist countermeasures.
In a new paper, by University of Wisconsin-Madison researcher Caitlin Pepperell, the research describes a bacterium that marches in lockstep with human population growth and history, evolving to take advantage of the most crowded and wretched human conditions.
The historical research reveals that tuberculosis experienced a 25-fold expansion worldwide in the 17th century, a time when human populations underwent explosive growth and European exploration of Africa, the Americas, Asia and Oceania was at its peak.
TB is only transmitted by people, and the organism cannot survive in the environment. It thrives, however, in the crowded conditions of prisons, refugee camps and slums, and TB populations tend to be dominated by the bacteria "lucky" enough to land in those environments.
The analysis focused on the role of natural selection, looking at patterns of genetic diversity among 63 TB and related pathogenic mycobacterial genomes gathered from around the globe. The study shows a highly constrained bacterial genome, with most deleterious mutations quickly discarded. This was especially true for genes essential for causing disease, protein translation and the trafficking and metabolism of inorganic ions, which help control the interaction between the TB pathogen and its human host. The bacterium's "defense" genes, on the other hand, showed a high degree of tolerance for beneficial mutations, which may play a role in evolution of drug resistance and evasion of the human immune system.
To read more, refer to the following paper:
Caitlin S. Pepperell, Amanda M. Casto, Andrew Kitchen, Julie M. Granka, Omar E. Cornejo, Eddie C. Holmes, Bruce Birren, James Galagan, Marcus W. Feldman. The Role of Selection in Shaping Diversity of Natural M. tuberculosis Populations. PLoS Pathogens, 2013; 9 (8): e1003543 DOI: 10.1371/journal.ppat.1003543
Posted by Tim Sandle
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