A hallmark feature of severe Group A Streptococcus pyogenes (GAS) infection is dysregulated
hemostasis. Hemostasis is the primary pathway for regulating blood flow through events that
contribute towards clot formation and its dissolution. However, a number of studies have identified
components of hemostasis in regulating survival and dissemination of GAS. Several proteins have
been identified on the surface of GAS and they serve to either facilitate invasion to host distal sites or
regulate inflammatory responses to the pathogen. GAS M-protein, a surface-exposed virulence factor,
appears to be a major target for interactions with host hemostasis proteins. These interactions mediate
biochemical events both on the surface of GAS and in the solution when M-protein is released into the
surrounding environment through shedding or regulated proteolytic processes that dictate the fate of
this pathogen. A thorough understanding of the mechanisms associated with these interactions could
lead to novel approaches for altering the course of GAS pathogenicity.
Keywords: Group A Streptococcus, hemostasis, inflammation, pyogenes, pathogen, M-protein.
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