Multilocus analysis of extracellular putative virulence proteins made by group A
            <i>Streptococcus:</i>
            Population genetics, human serologic response, and gene transcription

Reid, Sean D.; Green, Nicole M.; Buss, Julie K.; Lei, Benfang; Musser, James M.

doi:10.1073/pnas.121188598

Cited by 45 publications

(57 citation statements)

References 60 publications

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“…These data fit with the epidemiological observation of an association between the M serotype and certain pathological conditions in humans and mice (158). On the other hand, a detailed analysis of DNA sequence polymorphism of the set of chromosomal virulence genes studied by Reid et al (192) revealed numerous likely horizontal transfer events between the different M strains, and the authors suspected that generalized phage transduction was responsible for at least some of these gene transfers.…”

Section: Vol 68 2004 Phages and The Evolution Of Bacterial Pathogensupporting

confidence: 81%

“…16A). Sequence analysis of 10 chromosomally encoded fitness factors (extracellular proteins) revealed a striking correlation with the M serotypes of these strains (192). These observations suggest that the S. pyogenes strains (M serotypes) have evolved as distinct pathovars, harboring a specific set of chromosomally encoded fitness factors.…”

Section: Vol 68 2004 Phages and The Evolution Of Bacterial Pathogenmentioning

confidence: 82%

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Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion

Brüssow

Canchaya

Hardt

2004

Microbiol Mol Biol Rev

1,455

1,295

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Comparative genomics demonstrated that the chromosomes from bacteria and their viruses (bacteriophages) are coevolving. This process is most evident for bacterial pathogens where the majority contain prophages or phage remnants integrated into the bacterial DNA. Many prophages from bacterial pathogens encode virulence factors. Two situations can be distinguished: Vibrio cholerae, Shiga toxin-producing Escherichia coli, Corynebacterium diphtheriae, and Clostridium botulinum depend on a specific prophage-encoded toxin for causing a specific disease, whereas Staphylococcus aureus, Streptococcus pyogenes, and Salmonella enterica serovar Typhimurium harbor a multitude of prophages and each phage-encoded virulence or fitness factor makes an incremental contribution to the fitness of the lysogen. These prophages behave like “swarms” of related prophages. Prophage diversification seems to be fueled by the frequent transfer of phage material by recombination with superinfecting phages, resident prophages, or occasional acquisition of other mobile DNA elements or bacterial chromosomal genes. Prophages also contribute to the diversification of the bacterial genome architecture. In many cases, they actually represent a large fraction of the strain-specific DNA sequences. In addition, they can serve as anchoring points for genome inversions. The current review presents the available genomics and biological data on prophages from bacterial pathogens in an evolutionary framework

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Section: Vol 68 2004 Phages and The Evolution Of Bacterial Pathogensupporting

confidence: 81%

Section: Vol 68 2004 Phages and The Evolution Of Bacterial Pathogenmentioning

confidence: 82%

Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion

Brüssow

Canchaya

Hardt

2004

Microbiol Mol Biol Rev

1,455

1,295

View full text Add to dashboard Cite

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“…1B). To determine whether antibody alone promoted adherence of the bacteria to the A549 cells, strain MGAS5005 was incubated with A549 cells in the presence of affinity-purified rabbit antibody raised against Spy0843, a protein present on the cell surface of strain MGAS5005 (12). The antibody to Spy0843 had no effect on adherence of strain MGAS5005.…”

Section: Antibody To Sic Abrogates the Inhibition Of Adherence Of Sermentioning

confidence: 99%

Insight into the molecular basis of pathogen abundance: Group AStreptococcusinhibitor of complement inhibits bacterial adherence and internalization into human cells

Hoe

Ireland

DeLeo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Streptococcal inhibitor of complement (Sic) is a secreted protein made predominantly by serotype M1 Group A Streptococcus (GAS), which contributes to persistence in the mammalian upper respiratory tract and epidemics of human disease. Unexpectedly, an isogenic sic-negative mutant adhered to human epithelial cells significantly better than the wild-type parental strain. Purified Sic inhibited the adherence of a sic negative serotype M1 mutant and of non-Sic-producing GAS strains to human epithelial cells. Sic was rapidly internalized by human epithelial cells, inducing cell flattening and loss of microvilli. Ezrin and moesin, human proteins that functionally link the cytoskeleton to the plasma membrane, were identified as Sic-binding proteins by affinity chromatography and matrix-assisted laser desorption͞ionization time-of-flight mass spectrometry analysis. Sic colocalized with ezrin inside epithelial cells and bound to the F-actin-binding site region located in the carboxyl terminus of ezrin and moesin. Synthetic peptides corresponding to two regions of Sic had GAS adherence-inhibitory activity equivalent to mature Sic and inhibited binding of Sic to ezrin. In addition, the sic mutant was phagocytosed and killed by human polymorphonuclear leukocytes significantly better than the wild-type strain, and Sic colocalized with ezrin in discrete regions of polymorphonuclear leukocytes. The data suggest that binding of Sic to ezrin alters cellular processes critical for efficient GAS contact, internalization, and killing. Sic enhances bacterial survival by enabling the pathogen to avoid the intracellular environment. This process contributes to the abundance of M1 GAS in human infections and their ability to cause epidemics. microbiology ͉ Serotype M1 ͉ epidemic waves ͉ ezrin F or most bacterial pathogens, there is relatively little understanding of why certain clonally related isolates cause abundant infections, whereas others do not. Molecular explanation of these phenomena is critical to development of rational methods to limit pathogen emergence, resurgence, and dissemination.Group A Streptococcus (GAS) is an important human pathogen that causes infections ranging from pharyngitis to necrotizing fasciitis and the postinfectious sequelae acute rheumatic fever and acute glomerulonephritis. GAS are genetically highly heterogeneous. For example, more than 150 distinct M-types have been identified on the basis of antigenic differences in the M protein, an antiphagocytic surface molecule that is an important virulence factor (1). However, GAS expressing relatively few M types cause the majority of human invasive infections. In particular, M1 strains are the most common serotype recovered from invasive disease episodes and also have a propensity to cause epidemics (2).Streptococcal inhibitor of complement (Sic) is a secreted protein produced by serotype M1 GAS that inhibits the formation of the membrane attack complex (MAC) of complement in vitro by binding to the C5b-C7 complex (3, 4). Sic production is necessary for per...

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“…Work in this area, from classic studies (5) to a number of recent discoveries (6), has shown that certain human polymorphisms, some of which are responsible for genetic diseases, are also associated with resistance to common infectious diseases. An equally important but as yet incipient area of research will elucidate how the genetic variation of pathogen populations (7)(8)(9)(10)(11)) is related to genetic structure among their human hosts (12)(13)(14). An initial step in this undertaking is to determine the nature and stability of associations between host and pathogen populations.…”

mentioning

confidence: 99%

Stable association between strains of Mycobacterium tuberculosis and their human host populations

Hirsh

Tsolaki

DeRiemer

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

377

321

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Mycobacterium tuberculosis is an important human pathogen in virtually every part of the world. Here we investigate whether distinct strains of M. tuberculosis infect different human populations and whether associations between host and pathogen populations are stable despite global traffic and the convergence of diverse strains of the pathogen in cosmopolitan urban centers. The recent global movement and transmission history of 100 M. tuberculosis isolates was inferred from a molecular epidemiologic study of tuberculosis that spans 12 years. Genetic relationships among these isolates were deduced from the distribution of large genomic deletions, which were identified by DNA microarray and confirmed by PCR and sequence analysis. Phylogenetic analysis of these deletions indicates that they are unique event polymorphisms and that horizontal gene transfer is extremely rare in M. tuberculosis. In conjunction with the epidemiological data, phylogenies reveal three large phylogeographic regions. A host's region of origin is predictive of the strain of tuberculosis he or she carries, and this association remains strong even when transmission takes place in a cosmopolitan urban center outside of the region of origin. Approximate dating of the time since divergence of East Asian and Philippine clades of M. tuberculosis suggests that these lineages diverged centuries ago. Thus, associations between host and pathogen populations appear to be highly stable.M ycobacterium tuberculosis is a global pathogen, killing 1.9 million people each year and infecting Ϸ2 billion people worldwide (1, 2). Although it is primarily a scourge of the developing world, tuberculosis affects virtually every nation and every ethnicity (2). In view of this ubiquity, an important question in understanding the epidemiology and basic disease biology of the current pandemic is whether there are geographically or ethnically defined human populations within which transmission of M. tuberculosis is relatively common but between which transmission is far more limited. Do global traffic and ''small world'' effects result in a single, panmictic population of M. tuberculosis, or is the pathogen population somehow subdivided, with genetically distinct varieties carried in distinct populations of human hosts?The answer to this basic question may have direct implications for the development and administration of tuberculosis vaccines. Genetic variability in the pathogen population, as in Plasmodium and Streptococcus pneumoniae, can render vaccines ineffective against certain strains or in certain geographic regions. There is substantial geographic variability in the efficacy of the world's current tuberculosis vaccine (3, 4), and the reasons for this variation are not yet well understood. Although it is possible that genetic differences among strains of M. tuberculosis play a role in the variable efficacy of bacillus Calmette-Guérin, actual associations between distinct strains of M. tuberculosis and their human host populations have not been demonstrated, and ...

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Multilocus analysis of extracellular putative virulence proteins made by group A Streptococcus: Population genetics, human serologic response, and gene transcription

Cited by 45 publications

References 60 publications

Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion

Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion

Insight into the molecular basis of pathogen abundance: Group AStreptococcusinhibitor of complement inhibits bacterial adherence and internalization into human cells

Stable association between strains of Mycobacterium tuberculosis and their human host populations

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