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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2016,5,31]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    is a major cause of life-threatening bacterial infection. A significant risk factor for infection is nasal carriage. Previously, we reported spontaneous mutations during carriage associated with infection, including loss-of-function of the gene\n                    <jats:italic>repressor of surface proteins<\/jats:italic>\n                    (\n                    <jats:italic>rsp<\/jats:italic>\n                    ). Here we use genomic screens, experimental assays, and molecular examination of\n                    <jats:italic>rsp<\/jats:italic>\n                    mutants from patients to understand how\n                    <jats:italic>rsp<\/jats:italic>\n                    is involved in infection; we find it has far-reaching effects on gene regulation. Paradoxically,\n                    <jats:italic>rsp<\/jats:italic>\n                    mutants exhibited attenuated toxicity and reduced disease severity early in experimental infection, without sacrificing the ability to cause abscesses and bloodstream infection. This work reveals a complex relationship between correlates of disease in the laboratory and in patients, demonstrating that life-threatening disease can be associated with reduced severity early in infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1520255113","type":"journal-article","created":{"date-parts":[[2016,5,16]],"date-time":"2016-05-16T22:50:34Z","timestamp":1463439034000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":108,"title":["Natural mutations in a\n                    <i>Staphylococcus aureus<\/i>\n                    virulence regulator attenuate cytotoxicity but permit bacteremia and abscess formation"],"prefix":"10.1073","volume":"113","author":[{"given":"Sudip","family":"Das","sequence":"first","affiliation":[{"name":"Biocenter, Chair of Microbiology, University of W\u00fcrzburg, D-97074 Wuerzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudia","family":"Lindemann","sequence":"additional","affiliation":[{"name":"Jenner Institute, Centre for Molecular and Cellular Physiology, Oxford OX3 7BN, United Kingdom;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernadette C.","family":"Young","sequence":"additional","affiliation":[{"name":"Nuffield Department of Medicine, University of Oxford, Oxford OX3 7BN, United Kingdom;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julius","family":"Muller","sequence":"additional","affiliation":[{"name":"Jenner Institute, Centre for Molecular and Cellular Physiology, Oxford OX3 7BN, United Kingdom;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Babett","family":"\u00d6sterreich","sequence":"additional","affiliation":[{"name":"Institute of Molecular Infection Biology, University of W\u00fcrzburg, D-97080 Wuerzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola","family":"Ternette","sequence":"additional","affiliation":[{"name":"Jenner Institute, Centre for Molecular and Cellular Physiology, Oxford OX3 7BN, United Kingdom;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann-Cathrin","family":"Winkler","sequence":"additional","affiliation":[{"name":"Biocenter, Chair of Microbiology, University of W\u00fcrzburg, D-97074 Wuerzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kerstin","family":"Paprotka","sequence":"additional","affiliation":[{"name":"Biocenter, Chair of Microbiology, University of W\u00fcrzburg, D-97074 Wuerzburg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Reinhardt","sequence":"additional","affiliation":[{"name":"Max Planck Genome Centre, D-50829 Cologne, 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J Innate Immun 2, 576\u2013586 (2010).","journal-title":"J Innate Immun"},{"key":"e_1_3_4_6_2","doi-asserted-by":"crossref","first-page":"863","DOI":"10.1126\/science.1242255","article-title":"Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death","volume":"342","author":"Thammavongsa V","year":"2013","unstructured":"V Thammavongsa, DM Missiakas, O Schneewind, Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death. Science 342, 863\u2013866 (2013).","journal-title":"Science"},{"key":"e_1_3_4_7_2","doi-asserted-by":"crossref","first-page":"132","DOI":"10.1038\/nrmicro1824","article-title":"Complement evasion by human pathogens","volume":"6","author":"Lambris JD","year":"2008","unstructured":"JD Lambris, D Ricklin, BV Geisbrecht, Complement evasion by human pathogens. 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Microbiol Mol Biol Rev 78, 199\u2013230 (2014).","journal-title":"Microbiol Mol Biol Rev"},{"key":"e_1_3_4_11_2","doi-asserted-by":"crossref","first-page":"753","DOI":"10.1016\/S0140-6736(02)07877-7","article-title":"Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients","volume":"359","author":"Gillet Y","year":"2002","unstructured":"Y Gillet, , Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. 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