ArticleInfection and immunity2000
Absence of SpeB production in virulent large capsular forms of group A streptococcal strain 64.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Immunomodulating Enzymes fromMicroorganisms · 2024Review
- Streptolysin O concentration and activity is central to in vivo phenotype and disease outcome in Group A Streptococcus infection.Scientific reports · 2021Article
- Genetic switch to hypervirulence reduces colonization phenotypes of the globally disseminated group A streptococcus M1T1 clone.The Journal of infectious diseases · 2010Article
- Streptococcal inhibitor of complement promotes innate immune resistance phenotypes of invasive M1T1 group A Streptococcus.Journal of innate immunity · 2010Article
- Generation of metabolically diverse strains of Streptococcus pyogenes during survival in stationary phase.Journal of bacteriology · 2009Article
- Induction of group A Streptococcus virulence by a human antimicrobial peptide.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Analysis of the transcriptome of group A Streptococcus in mouse soft tissue infection.The American journal of pathology · 2006Article
- Streptococcal pyrogenic exotoxin B causes mitochondria damage to polymorphonuclear cells preventing phagocytosis of group A streptococcus.Medical microbiology and immunology · 2006Article
- Viable group A streptococci in macrophages during acute soft tissue infection.PLoS medicine · 2006Article
- Genome-wide analysis of group a streptococci reveals a mutation that modulates global phenotype and disease specificity.PLoS pathogens · 2006Article
- Group A Streptococcus transcriptome dynamics during growth in human blood reveals bacterial adaptive and survival strategies.The American journal of pathology · 2005Article
- Streptococcus pyogenes infection in mouse skin leads to a time-dependent up-regulation of protein H expression.Infection and immunity · 2003Article
- Cleavage of antigen-bound immunoglobulin G by SpeB contributes to streptococcal persistence in opsonizing blood.Infection and immunity · 2003Article
- Role of CsrR, hyaluronic acid, and SpeB in the internalization of Streptococcus pyogenes M type 3 strain by epithelial cells.Infection and immunity · 2002Article
- Mouse skin passage of a Streptococcus pyogenes Tn917 mutant of sagA/pel restores virulence, beta-hemolysis and sagA/pel expression without altering the position or sequence of the transposon.BMC microbiology · 2001Article
- Inverse relation between disease severity and expression of the streptococcal cysteine protease, SpeB, among clonal M1T1 isolates recovered from invasive group A streptococcal infection cases.Infection and immunity · 2000Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Passage in human blood of group A streptococcal isolate 64p was previously shown to result in the enhanced expression of M and M-related proteins. Similarly, when this isolate was injected into mice via an air sac model for skin infection, organisms recovered from the spleens showed both increased expression of M and M-related proteins and increased skin-invasive potential. We show that these phenotypic changes were not solely the result of increased transcription of the mRNAs encoding the M and M-related gene products. Rather, the altered expression was associated with posttranslational modifications of the M and M-related proteins that occur in this strain, based on the presence or absence of another virulence protein, the streptococcal cysteine protease SpeB. The phenotypic variability also correlates with colony size variation. Large colonies selected by both regimens expressed more hyaluronic acid, which may explain differences in colony morphology. All large-colony variants were SpeB negative and expressed three distinct immunoglobulin G (IgG)-binding proteins in the M and M-related protein family. Small-colony variants were SpeB positive and bound little IgG through their M and M-related proteins because these proteins, although made, were degraded or altered in profile by the SpeB protease. We conclude that passage in either human blood or a mouse selects for a stable, phase-varied strain of group A streptococci which is altered in many virulence properties.
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