A decade of molecular pathogenomic analysis of group A Streptococcus
James M. Musser, Samuel A. Shelburne III
James M. Musser, Samuel A. Shelburne III
Published September 1, 2009
Citation Information: J Clin Invest. 2009;119(9):2455-2463. https://doi.org/10.1172/JCI38095.
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A decade of molecular pathogenomic analysis of group A Streptococcus

Abstract

Molecular pathogenomic analysis of the human bacterial pathogen group A Streptococcus has been conducted for a decade. Much has been learned as a consequence of the confluence of low-cost DNA sequencing, microarray technology, high-throughput proteomics, and enhanced bioinformatics. These technical advances, coupled with the availability of unique bacterial strain collections, have facilitated a systems biology investigative strategy designed to enhance and accelerate our understanding of disease processes. Here, we provide examples of the progress made by exploiting an integrated genome-wide research platform to gain new insight into molecular pathogenesis. The studies have provided many new avenues for basic and translational research.

Authors

James M. Musser, Samuel A. Shelburne III

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Figure 2

The role of the CovR/S TCS in the transition from mucosal to invasive disease.

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The role of the CovR/S TCS in the transition from mucosal to invasive di...
(A) Upon entering subcutaneous tissue, GAS is confronted by neutrophils that produce NETs. (B–D) Mutation in the CovR/S TCS (B) allows for high-level production of a GAS DNase that degrades NETs (C), thereby increasing pathogen survival and enhancing the probability of invasive infection (D). (E) Principal component analysis of expression microarray data demonstrates that mucosal (or pharyngeal) and invasive GAS isolates have strikingly different transcriptomes. (F) Examples of genes encoding critical virulence factors that are more highly expressed in invasive isolates (red) or pharyngeal isolates (blue). ITP, invasive transcriptome profile; PTP, pharyngeal transcriptome profile. A–D are reprinted with permission from Nature Medicine (93). E and F are adapted from PLoS Pathogens (92).