TY - JOUR
T1 - Molecular characterization of an invasive phenotype of group a streptococcus arising during human infection using whole genome sequencing of multiple isolates from the same patient
AU - Flores, Anthony R.
AU - Sahasrabhojane, Pranoti
AU - Saldaña, Miguel
AU - Galloway-Peña, Jessica
AU - Olsen, Randall J.
AU - Musser, James M.
AU - Shelburne, Samuel
N1 - Funding Information:
Financial support. This work was supported the National Institutes of Allergy and Infectious Diseases at the National Institutes of Health by [5R01AI089891 to S. A. S.]. A. R. F. is a scholar of the Harold Amos Medical Faculty Development Program. Potential conflicts of interest. All authors: No reported conflicts.
PY - 2014/5/15
Y1 - 2014/5/15
N2 - Invasive group A streptococcal (GAS) strains often have genetic differences compared to GAS strains from nonsterile sites. Invasive, " hypervirulent" GAS strains can arise from a noninvasive progenitor following subcutaneous inoculation in mice, but such emergence has been rarely characterized in humans. We used whole genome analyses of multiple GAS isolates from the same patient to document the molecular basis for emergence of a GAS strain with an invasive phenotype during human infection. In contrast to previous theories, we found that elimination of production of the cysteine protease SpeB was not necessary for emergence of GAS with an invasive, "hypervirulent" phenotype.
AB - Invasive group A streptococcal (GAS) strains often have genetic differences compared to GAS strains from nonsterile sites. Invasive, " hypervirulent" GAS strains can arise from a noninvasive progenitor following subcutaneous inoculation in mice, but such emergence has been rarely characterized in humans. We used whole genome analyses of multiple GAS isolates from the same patient to document the molecular basis for emergence of a GAS strain with an invasive phenotype during human infection. In contrast to previous theories, we found that elimination of production of the cysteine protease SpeB was not necessary for emergence of GAS with an invasive, "hypervirulent" phenotype.
KW - bacterial pathogenesis
KW - gene expression.
KW - group A Streptococcus
KW - virulence
KW - whole genome sequencing
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U2 - 10.1093/infdis/jit674
DO - 10.1093/infdis/jit674
M3 - Article
C2 - 24307742
AN - SCOPUS:84899515199
VL - 209
SP - 1520
EP - 1523
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 10
ER -