Abstract
Group A Streptococcus (GAS) causes common pharyngitis and skin infections and occasional severe invasive infections. This review describes the recent progress on the pathogenesis of hypervirulent GAS. CovRS mutations are frequent among invasive GAS isolates and lead to hypervirulence. GAS CovRS mutants can be selected in vivo by neutrophils. The role of protease SpeB in source-sink dynamics of wild-type GAS and hypervirulent variants is discussed. Streptolysin S and PAF acetylhydrolase Sse critically and synergistically contribute to the inhibition of neutrophil recruitment by GAS CovS mutants. CovS mutations in emm3 GAS lead to the vascular invasion and enhance systemic GAS dissemination.
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