DRS Is Far Less Divergent than Streptococcal Inhibitor of Complement of Group A Streptococcus

Sagar, Vivek; Kumar, Rajesh; Ganguly, Nirmal Kumar; Menon, Thangam; Chakraborti, Anuradha

doi:10.1128/jb.01619-06

Cited by 5 publications

(4 citation statements)

References 15 publications

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“…Streptococcal inhibitor of complement (SIC) and distantly related to SIC (DRS) are some extent of homology. DRS binds complement factors but does not inhibit complement mediated cell lysis [ 56 , 57 ], whereas SIC inhibits complement mediated cell lysis [ 58 ]. GGS_124 harbors a putative DRS gene (SDEG_0932), which consists of a signal sequence, two repeat regions, and a proline-rich region typical of DRS, and is homologous to the Drs12.04 protein of GAS strain emm12 with 48% amino acid identity [ 59 ] (Additional file 6 ).…”

Section: Resultsmentioning

confidence: 99%

Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS)

et al. 2011

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BackgroundStreptococcus dysgalactiae subsp. equisimilis (SDSE) causes invasive streptococcal infections, including streptococcal toxic shock syndrome (STSS), as does Lancefield group A Streptococcus pyogenes (GAS). We sequenced the entire genome of SDSE strain GGS_124 isolated from a patient with STSS.ResultsWe found that GGS_124 consisted of a circular genome of 2,106,340 bp. Comparative analyses among bacterial genomes indicated that GGS_124 was most closely related to GAS. GGS_124 and GAS, but not other streptococci, shared a number of virulence factor genes, including genes encoding streptolysin O, NADase, and streptokinase A, distantly related to SIC (DRS), suggesting the importance of these factors in the development of invasive disease. GGS_124 contained 3 prophages, with one containing a virulence factor gene for streptodornase. All 3 prophages were significantly similar to GAS prophages that carry virulence factor genes, indicating that these prophages had transferred these genes between pathogens. SDSE was found to contain a gene encoding a superantigen, streptococcal exotoxin type G, but lacked several genes present in GAS that encode virulence factors, such as other superantigens, cysteine protease speB, and hyaluronan synthase operon hasABC. Similar to GGS_124, the SDSE strains contained larger numbers of clustered, regularly interspaced, short palindromic repeats (CRISPR) spacers than did GAS, suggesting that horizontal gene transfer via streptococcal phages between SDSE and GAS is somewhat restricted, although they share phage species.ConclusionGenome wide comparisons of SDSE with GAS indicate that SDSE is closely and quantitatively related to GAS. SDSE, however, lacks several virulence factors of GAS, including superantigens, SPE-B and the hasABC operon. CRISPR spacers may limit the horizontal transfer of phage encoded GAS virulence genes into SDSE. These findings may provide clues for dissecting the pathological roles of the virulence factors in SDSE and GAS that cause STSS.

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Section: Resultsmentioning

confidence: 99%

Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS)

et al. 2011

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“…S. pyogenes strains express a multitude of genes coding for DNases, antibiotic resistance and the highly virulent superantigens that cause streptococcal toxic shock syndrome in addition to other nonsuppurative sequelae (Aziz & Kotb, 2008). S. pyogenes also exhibits C5a peptidase, streptolysin O and streptolysin S activity, which aid in streptococcal cytotoxicity and virulence (Sagar et al, 2008). The S. pyogenes M protein is probably the most notorious virulence factor that this micro-organism possesses.…”

Section: Introductionmentioning

confidence: 99%

emm typing, antibiotic resistance and PFGE analysis of Streptococcus pyogenes in Lebanon

Bahnan

Hashwa

Araj

et al. 2011

Journal of Medical Microbiology

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One hundred and three Streptococcus pyogenes isolates recovered mainly from streptococcal throat infections in Lebanon were characterized by emm and PFGE typing. Thirty-three emm types and subtypes were detected among the isolates. PFGE was more discriminatory as a typing method. The prevalent emm types were emm1 (12.6 %), emm22 (8.7 %), emm28 (7.7 %), emm88 (7.7 %) and emm4 (6.8 %) and all isolates were susceptible to vancomycin and penicillin G. Ten per cent of the isolates were resistant to erythromycin and 3 % were resistant to erythromycin and clindamycin, showing the macrolide-lincosamide-streptogramin B phenotype. The emm sequences and PFGE pattern database that were generated in this study will serve as a basis for information for long-term evolutionary and epidemiological studies of local S. pyogenes recovered not only in Lebanon, but also in neighbouring countries. INTRODUCTIONStreptococcus pyogenes is one of the most clinically important Gram-positive pathogens. S. pyogenes causes disease states that vary between mild sore throat to the flesh-eating disease necrotizing fasciitis. S. pyogenes causes, other than the acute diseases, a set of severe post-disease sequelae such as rheumatic fever and post-streptococcal glomerulonephritis (Yoonim et al., 2005).The successful nature of S. pyogenes as a pathogen relates to its wide array of virulence factors, be they secreted or cell bound. S. pyogenes strains express a multitude of genes coding for DNases, antibiotic resistance and the highly virulent superantigens that cause streptococcal toxic shock syndrome in addition to other nonsuppurative sequelae (Aziz & Kotb, 2008). S. pyogenes also exhibits C5a peptidase, streptolysin O and streptolysin S activity, which aid in streptococcal cytotoxicity and virulence (Sagar et al., 2008). The S. pyogenes M protein is probably the most notorious virulence factor that this micro-organism possesses. It is a fibrillar cell wall protein that aids in adherence to human cells and prevention of opsonophagocytosis. This protein, due to molecular mimicry within protein sequences found in human tissues, is implicated in rheumatic fever (Guilherme et al., 2006). S. pyogenes emm typing has become one of the best approaches used in molecular typing of this microorganism. Many methods have been exploited to best type S. pyogenes, such as 16S rRNA gene sequencing (Stanley et al., 1995), restriction fragment length polymorphism analysis (Desai et al., 1999), random amplified polymorphic DNA analysis (Seppälä et al., 1994) and PFGE (Chiou et al., 2004). However, sequencing-based emm typing by the use of oligonucleotides that target the Nterminus of the M-protein coding gene remains the most practical method of S. pyogenes typing (Beall et al., 2000). The reason behind this is that the gene coding for the group A Streptococcus M protein contains a hypervariable 59 region that is subject to many single nucleotide polymorphisms, which serves as the basis for emm typing S. pyogenes isolates (Yoonim et al., 2005).To our knowledge, this ...

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“…SIC and DRS antibodies are persistent, and overwhelming evidence show that the distribution of the SIC and DRS genes is restricted to mainly four emm types [ 7 , 8 , 19 ]. The isolation rate of these four types from our pyoderma cohort is low (<5%), and our previous study from this region also show that these types are recovered in low numbers in Mumbai population [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Antibodies to group A streptococcal virulence factors, SIC and DRS, increase predilection to GAS pyoderma

et al. 2015

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BackgroundStreptococcus pyogenes (group A streptococcus; GAS) is an etiological agent for pharyngitis, pyoderma, and invasive infections in humans. Pharyngitis and pyoderma may lead to serious immune sequelae such as rheumatic heart disease and post-streptococcal glomerulonephritis (PSGN). Streptococcal Inhibitor of Complement (SIC) and its orthologue, distantly related to SIC (DRS), are virulence factors expressed by only four of more than 100 M types of GAS. These four types (M1, M57, M12 and M55) are among the M types, which are associated with PSGN. In several populations PSGN has been shown to be a risk factor for chronic kidney disease (CKD) and end-stage renal disease (ESRD). Previous studies showed SIC or DRS antibody-prevalence was associated with PSGN, and seroprevalence of SIC antibodies is significantly high among CKD and ESRD patients in Mumbai.MethodsStreptococcal isolates recovered from GAS pyoderma cases were typed. Seropositivity for SIC and DRS antibodies in subjects with pyoderma, PSGN pediatric cases, age matched healthy controls and non-GAS pyoderma cases were determined.ResultsWe confirm in this study an association between seroprevalence to SIC and DRS antibodies, and PSGN in Mumbai population despite low point prevalence of M1, M12, M55 and M57. In addition we extended the study to GAS-pyoderma and non-GAS pyoderma cases. To our surprise, we found a positive association between the seroprevalence to SIC and DRS antibodies, and GAS-pyoderma owing to infection with diverse M types. The mechanism of increased predisposition to pyoderma owing to infection by diverse GAS among SIC or DRS antibody-positive population is not clear. Nonetheless, our findings could be explained by a phenomenon akin to antibody-dependent enhancement (ADE).ConclusionsThis is the first report showing a small number of GAS M types conferring predisposition to pyoderma by diverse types. Implications of this ADE-like phenomenon are discussed in the light of evolutionary advantage to GAS, vaccine design and control of renal diseases.

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DRS Is Far Less Divergent than Streptococcal Inhibitor of Complement of Group A Streptococcus

Cited by 5 publications

References 15 publications

Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS)

Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS)

emm typing, antibiotic resistance and PFGE analysis of Streptococcus pyogenes in Lebanon

Antibodies to group A streptococcal virulence factors, SIC and DRS, increase predilection to GAS pyoderma

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