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10.1172/JCI82478 http://scihub22266oqcxt.onion/10.1172/JCI82478 C4588293!4588293!26258415     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (9): 3545-59 Nephropedia Template TP {{tp|p=26258415|t=2015. A molecular trigger for intercontinental epidemics of group A Streptococcus |pdf=|usr=}}{{26258415}} gab.com Text A molecular trigger for intercontinental epidemics of group A Streptococcus JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26258415 #FOAvip The identification of the molecular events responsible for strain emergence, enhanced virulence, and epidemicity has been a long-pursued goal in infectious diseases research. A recent analysis of 3,615 genomes of serotype M1 group A Streptococcus strains (the so-called ?flesh-eating? bacterium) identified a recombination event that coincides with the global M1 pandemic beginning in the early 1980s. Here, we have shown that the allelic variation that results from this recombination event, which replaces the chromosomal region encoding secreted NADase and streptolysin O, is the key driver of increased toxin production and enhanced infection severity of the M1 pandemic strains. Using isoallelic mutant strains, we found that 3 polymorphisms in this toxin gene region increase resistance to killing by human polymorphonuclear leukocytes, increase bacterial proliferation, and increase virulence in animal models of pharyngitis and necrotizing fasciitis. Genome sequencing of an additional 1,125 streptococcal strains and virulence studies revealed that a highly similar recombinational replacement event underlies an ongoing intercontinental epidemic of serotype M89 group A Streptococcus infections. By identifying the molecular changes that enhance upper respiratory tract fitness, increased resistance to innate immunity, and increased tissue destruction, we describe a mechanism that underpins epidemic streptococcal infections, which have affected many millions of people. Twit Text FOAVip A molecular trigger for intercontinental epidemics of group A Streptococcus ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26258415 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26258415 #FOAvip English Wikipedia <ref>{{Cite pmid|26258415}}</ref> A molecular trigger for intercontinental epidemics of group A Streptococcus #MMPMID26258415 Zhu L; Olsen RJ; Nasser W; Beres SB; Vuopio J; Kristinsson KG; Gottfredsson M; Porter AR; DeLeo FR; Musser JM J Clin Invest 2015[Sep]; 125 (9): 3545-59 PMID26258415show ga The identification of the molecular events responsible for strain emergence, enhanced virulence, and epidemicity has been a long-pursued goal in infectious diseases research. A recent analysis of 3,615 genomes of serotype M1 group A Streptococcus strains (the so-called ?flesh-eating? bacterium) identified a recombination event that coincides with the global M1 pandemic beginning in the early 1980s. Here, we have shown that the allelic variation that results from this recombination event, which replaces the chromosomal region encoding secreted NADase and streptolysin O, is the key driver of increased toxin production and enhanced infection severity of the M1 pandemic strains. Using isoallelic mutant strains, we found that 3 polymorphisms in this toxin gene region increase resistance to killing by human polymorphonuclear leukocytes, increase bacterial proliferation, and increase virulence in animal models of pharyngitis and necrotizing fasciitis. Genome sequencing of an additional 1,125 streptococcal strains and virulence studies revealed that a highly similar recombinational replacement event underlies an ongoing intercontinental epidemic of serotype M89 group A Streptococcus infections. By identifying the molecular changes that enhance upper respiratory tract fitness, increased resistance to innate immunity, and increased tissue destruction, we describe a mechanism that underpins epidemic streptococcal infections, which have affected many millions of people. äA molecular trigger for intercontinental epidemics of group A Streptoc(epmc).pdf DeepDyve Pubget Overpricing