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Staphylococcus aureus  is a significant cause of human infection. Here, we demonstrate that mutations in the transcriptional repressor of purine biosynthesis,  purR , enhance the pathogenic potential of  S. aureus . Indeed, systemic infection with  purR  mutants causes accelerated mortality in mice, which is due to aberrant up-regulation of fibronectin binding proteins (FnBPs). Remarkably,  purR  mutations can arise upon exposure of  S. aureus  to stress, such as an intact immune system. In humans, naturally occurring anti-FnBP antibodies exist that, while not protective against recurrent  S. aureus  infection, ostensibly protect against hypervirulent  S. aureus  infections. Vaccination studies support this notion, where anti-Fnb antibodies in mice protect against  purR  hypervirulence. These findings provide a novel link between purine metabolism and virulence in  S. aureus .

Stress-induced inactivation of the Staphylococcus aureus purine biosynthesis repressor leads to hypervirulence