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This Week in PLOS: Dec 19, 2016

In PLOS Pathogens, researchers from New York University and other centers in the US and Switzerland outline evolutionary patterns in Mycobacterium tuberculosis that are related to the tuberculosis-causing pathogen's genotype and pressure from the host immune system. By sequencing their own M. tuberculosis lab strain and comparing it with the reference sequence for the virulent H37Rv strain, the investigators characterized genetic variants that appear to contribute to mouse host adaptation by the pathogen, as well as shifts in genetic diversity that coincided with M. tuberculosis growth in mice with or without immune T cells. "Together, our findings put M. tuberculosis genetic evolution in a new perspective and clarify the impact of T cells on sequence diversity of M. tuberculosis," they write.

A PLOS One paper looks at the genetic variation found in human papillomavirus isolates from the HPV52 genotype that were isolated from cervical samples in women from a Korean hospital. The research team, from South Korea and Hong Kong, did genome sequencing on 91 HPV52-positive samples: seven squamous cell carcinoma cases, 21 high-grade lesions, 22, low-grade lesions, and 40 isolates from symptom-free women. In the process, the group identified four HPV52 lineages, with most isolates falling into the B or C lineage. Moreover, the study's authors note that the lineages "harbored distinct genetic alterations that may affect oncogenicity." "Our findings increase our understanding on the heterogeneity of HPV52 variants," they write, "and may be useful for the development of new diagnostic assays and therapeutic vaccines."

Stanford University's Jonathan Pritchard and colleagues report on mutation rate variation patterns in humans for a study appearing in PLOS Genetics. By analyzing site frequency spectrum data for almost 61,000 individuals in version 2.0 of the Exome Aggregation Consortium, together with human, chimpanzee, gorilla, and other primate genome sequences, the team saw signs that human variants tended to turn up at higher frequency when also found independently in more closely related primates such as chimpanzees. On the other hand, the group's phylogenetically conditioned site frequency spectrum analysis suggested that when the substitutions were paralleled in primate with more distant ties to humans, the frequency typically dipped in humans. "[O]ur results suggest more variation in mutation rates across sites than is generally appreciated," the group writes, "and further that the infinite sites model provides a poor fit for population genetic analyses in large modern datasets."