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Figure 7 | BMC Genomics

Figure 7

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

Figure 7

Putative virulence factors and posited virulence function of SDSE. Cell-surface proteins, extracellular secreted proteins, metal transporters, and the two-component regulator CsrR/CsrS, which affect the expression of approximately 10% of all genes in a GAS strain [78, 79], are shown. The putative virulence factors on the cell surface of SDSE are adhesins, including M protein, fibronectin binding protein (Fbp), collagen binding protein (Cbp), laminin binding protein (Lbp), and pullulanase (Pul) [80]. Factors that protect bacteria from the host immune system are shown, including cell envelope proteinase A (CepA), which cleaves within the interleukin-8 (IL-8) C-terminal α-helix [38]; immunoglobulin G binding protein (GB) [49]; glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and C5a peptidase (Scp) [46]. Putative pathogenic roles of the virulence factors of SDSE, including hyaluronidase (Hyl), streptokinase (Ska), extracellular nuclease and streptodornase (DNase), which digest neutrophil extracellular traps (NETs) released from dead neutrophils [50], and the pore-forming proteins, such as hemolysin (Hly), streptolysin S (SLS), streptolysin O (SLO), and NAD glycohydrolase (NADase), are indicated. FtsABCD and HtsABC are ferrichrome transporters and MtsABC is a metal transporter. Black arrows show protein secretion, red arrows show expression of genes regulated by CsrR, blue arrows show protein attachment to the extracellular matrix, brown arrows show metal transport from the extracellular environment into the cell, and purple arrows show degradation of extracellular matrix by secreted Hyl or Ska. The factors marked with a Stop sign, which are major virulence factors of GAS, do not function in SDSE.

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