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Bacterial Pathogenesis Laboratory, The Queensland Institute of Medical Research, Brisbane 4029, Australia; The Australian Centre for International Tropical Health and Nutrition, The Queensland Institute of Medical Research, Brisbane 4029, Australia; Cooperative Research Centre for Vaccine Technology, The Queensland Institute of Medical Research, Brisbane 4029, Australia; National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, MB R3E 3R2 Canada; Faculty of Pharmacy, University of Manitoba, Winnipeg, MB R3T 2N2 Canada; Molecular Parasitology Laboratory, The Queensland Institute of Medical Research, Brisbane 4029, Australia
* To whom correspondence should be addressed. Email:
sriS{at}qimr.edu.au.
Streptococcus dysgalactiae subsp. equisimilis (group G streptococcus, GGS) are largely defined as commensal organisms, which are closely related to the well defined human pathogen, the group A streptococcus (GAS). While lateral gene transfers are emerging as a common theme between these species, little is known about the mechanisms and role of these transfers and their effect on the population structure of streptococci in nature. It is now becoming evident that bacteriophages are major contributors to the genotypic diversity of GAS and consequently, are pivotal to the GAS strain structure. Furthermore, bacteriophages are strongly associated with altering the pathogenic potential of GAS. In contrast, little is know about phages from GGS and their role in the population dynamics of GGS. In this study we report the first complete genome sequence of a GGS phage,
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Phage 3396 (
3396) from a Streptococcus dysgalactiae subspecies equisimilis pathovar may have its origins in S pyogenes
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Abstract
3396. Exhibiting high homology to the GAS phage
315.1, the chimeric nature of
3396 is unravelled to reveal evidence of extensive ongoing genetic diversity and dissemination of streptococcal phages in nature. Furthermore, we expand on our recent findings to identify inducible
3396-homologues in GAS from a region endemic for GAS and GGS infection. Together these findings provide new insights into the population structure of not only GGS, but the overall population structure of the streptococcal genus and the emergence of pathogenic variants.
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