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10.1128/IAI.00989-15 http://scihub22266oqcxt.onion/10.1128/IAI.00989-15 C4645388!4645388 !26416912     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26416912 &cmd=llinks): Failed to open stream: HTTP request failed! 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The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications |pdf=|usr=}}{{26416912 }} gab.com Text The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26416912 #FOAvip Group A streptococcus (GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine protease SpeB. Several lines of evidence suggest that SpeB is an important virulence factor. SpeB is expressed in human infections, protects mice from lethal challenge when used as a vaccine, and contributes significantly to tissue destruction and dissemination in animal models. However, recent descriptions of mutations in genes implicated in SpeB production have led to the idea that GAS may be under selective pressure to decrease secreted SpeB protease activity during infection. Thus, two divergent hypotheses have been proposed. One postulates that SpeB is a key contributor to pathogenesis; the other, that GAS is under selection to decrease SpeB during infection. In order to distinguish between these alternative hypotheses, we performed casein hydrolysis assays to measure the SpeB protease activity secreted by 6,775 GAS strains recovered from infected humans. The results demonstrated that 84.3% of the strains have a wild-type SpeB protease phenotype. The availability of whole-genome sequence data allowed us to determine the relative frequencies of mutations in genes implicated in SpeB production. The most abundantly mutated genes were direct transcription regulators. We also sequenced the genomes of 2,954 GAS isolates recovered from nonhuman primates with experimental necrotizing fasciitis. No mutations that would result in a SpeB-deficient phenotype were identified. Taken together, these data unambiguously demonstrate that the great majority of GAS strains recovered from infected humans secrete wild-type levels of SpeB protease activity. Our data confirm the important role of SpeB in GAS pathogenesis and help end a long-standing controversy. Twit Text FOAVip The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26416912 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26416912 #FOAvip English Wikipedia <ref>{{Cite pmid|26416912 }}</ref> The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications #MMPMID26416912 Olsen RJ ; Raghuram A ; Cantu C ; Hartman MH ; Jimenez FE ; Lee S ; Ngo A ; Rice KA ; Saddington D ; Spillman H ; Valson C ; Flores AR ; Beres SB ; Long SW ; Nasser W ; Musser JM Infect Immun 2015[Dec]; 83 (12 ): 4750-8 PMID26416912 show ga Group A streptococcus (GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine protease SpeB. Several lines of evidence suggest that SpeB is an important virulence factor. SpeB is expressed in human infections, protects mice from lethal challenge when used as a vaccine, and contributes significantly to tissue destruction and dissemination in animal models. However, recent descriptions of mutations in genes implicated in SpeB production have led to the idea that GAS may be under selective pressure to decrease secreted SpeB protease activity during infection. Thus, two divergent hypotheses have been proposed. One postulates that SpeB is a key contributor to pathogenesis; the other, that GAS is under selection to decrease SpeB during infection. In order to distinguish between these alternative hypotheses, we performed casein hydrolysis assays to measure the SpeB protease activity secreted by 6,775 GAS strains recovered from infected humans. The results demonstrated that 84.3% of the strains have a wild-type SpeB protease phenotype. The availability of whole-genome sequence data allowed us to determine the relative frequencies of mutations in genes implicated in SpeB production. The most abundantly mutated genes were direct transcription regulators. We also sequenced the genomes of 2,954 GAS isolates recovered from nonhuman primates with experimental necrotizing fasciitis. No mutations that would result in a SpeB-deficient phenotype were identified. Taken together, these data unambiguously demonstrate that the great majority of GAS strains recovered from infected humans secrete wild-type levels of SpeB protease activity. Our data confirm the important role of SpeB in GAS pathogenesis and help end a long-standing controversy. |*Gene Expression Regulation, Bacterial [MESH] |*Genome, Bacterial [MESH] |Animals [MESH] |Bacterial Proteins/*genetics/metabolism [MESH] |Caseins/chemistry [MESH] |Epidemiological Monitoring [MESH] |Europe/epidemiology [MESH] |Exotoxins/*genetics/metabolism [MESH] |Fasciitis, Necrotizing/epidemiology/microbiology/pathology [MESH] |High-Throughput Nucleotide Sequencing [MESH] |Humans [MESH] |Mutation [MESH] |Pharyngitis/epidemiology/microbiology/pathology [MESH] |Primates [MESH] |Proteolysis [MESH] |Serotyping [MESH] |Streptococcal Infections/epidemiology/microbiology/pathology [MESH] |Streptococcus pyogenes/classification/*enzymology/*genetics/pathogenicity [MESH] |Transcription, Genetic [MESH] |United States/epidemiology [MESH]The majority of 9,729 group A streptococcus strains causing disease se(epmc).pdf DeepDyve Pubget Overpricing