Table 1.
Alab49 mutants having a statistically significant decrease in virulence relative to wild-type, when tested in the humanized mouse model for superficial skin infection.
Mutant | Function of gene product | Control of gene transcription | Cell association | Virulence at skin (log inoculum)† | Virulence at skin (stat inoculum)† |
---|---|---|---|---|---|
Δmga | Transcriptional regulator | Autoregulated (activated)‡ | Cytoplasm | Decreased | Decreased |
Δnra | Transcriptional regulator | Autoregulated (activated)‡ | Cytoplasm | Decreased | Decreased |
Δpam (Δemm53) | Plg-binding M protein | Activated by mga | Surface | N.D. | Decreased (partially) |
Δska | Plg activator (streptokinase) | No effect by mga | Secreted | N.D. | Decreased (partially) |
ΔspeB | Cysteine protease | Activated by mga (indirect) | Secreted | Decreased | Decreased |
ΔfctA | Pilus backbone subunit | Activated by nra | Surface | No effect | No effect |
Δcpa | Collagen-binding protein (pilus) | Activated by nra | Surface | Decreased | No effect |
ΔprtF2 | Fn-binding protein | Activated by msmR | Surface | Decreased | No effect |
Virulence at the skin was measured for group A Streptococcus inoculum cultures grown to either log or stationary phase in enriched broth.
Assumed but not completely proven for strain Alab49; Mga and Nra function as autoregulators in other strains [37].
Fn: Fibronectin; N.D.: Not determined.