Abstract
Streptococcus pyogenes (group A streptococci; GAS) is an exclusively human pathogen. It causes a variety of suppurative and non-suppurative diseases in people of all ages worldwide. Not all can be successfully treated with antibiotics. A licensed vaccine, in spite of its global importance, is not yet available. GAS express an arsenal of virulence factors responsible for pathological immune reactions. The transcription of all these virulence factors is under the control of three types of virulence-related regulators: (i) two-component systems (TCS), (ii) stand-alone regulators, and (iii) non-coding RNAs. This review summarizes major TCS and stand-alone transcriptional regulatory systems, which are directly associated with virulence control. It is suggested that this treasure of knowledge on the genetics of virulence regulation should be better harnessed for new therapies and prevention methods for GAS infections, thereby changing its global epidemiology for the better.
Highlights
IntroductionA streptococcus” or “GAS”, based on the presence the group A cell wall polysaccharide antigen), is one of the most successful pathogens worldwide
Among the Gram-positive cocci, Streptococcus pyogenes, is one of the most successful pathogens worldwide
This review focuses on established virulence factors of GAS and their regulation, which play a major role in the different diseases caused by this versatile pathogen
Summary
A streptococcus” or “GAS”, based on the presence the group A cell wall polysaccharide antigen), is one of the most successful pathogens worldwide It causes superficial and deep (invasive) infections almost exclusively in humans. Late non-suppurative sequelae might appear weeks after a streptococcal infection, namely the acute rheumatic fever (ARF, including rheumatic heart disease—RHD [5]) primarily after throat infections or an acute glomerulonephritis (AGN, affecting the kidney) occurring after both streptococcal throat and skin infections [6] These sequelae are ascribed to autoimmune reactions directed against cross-reactive streptococcal antigens or neoantigens developing during an acute GAS infection [7]. Inhibitors or inducers of streptococcal quorum sensing systems may influence the GAS colonization status, either directly or indirectly through action on bacterial competitors in the throat or on the skin [38,39]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
