{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T15:28:40Z","timestamp":1775575720502,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,6,19]],"date-time":"2013-06-19T00:00:00Z","timestamp":1371600000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>As the <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>yme disease spirochaete <jats:italic><jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>orrelia burgdorferi<\/jats:italic> shuttles back and forth between arthropod vector and vertebrate host, it encounters vastly different and hostile environments. Major mechanisms contributing to the success of this pathogen throughout this complex transmission cycle are phase and antigenic variation of abundant and serotype\u2010defining surface lipoproteins. These peripherally membrane\u2010anchored virulence factors mediate niche\u2010specific interactions with vector\/host factors and protect the spirochaete from the perils of the mammalian immune response. In this issue of <jats:italic><jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>olecular <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>icrobiology<\/jats:italic>, <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>illy, <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>estor and <jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>osa redefine the roles of two lipoproteins, <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content>, during mammalian infection. Using a variety of promoter fusions in combination with a sensitive <jats:italic>in vivo<\/jats:italic> \u2018use it or lose it\u2019 gene complementation assay, the authors demonstrate that proper sequential expression of <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> followed by <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content> indeed matters. A previously suggested general functional redundancy between these and other lipoproteins is shown to be limited and dependent on an immunodeficient experimental setting that is arguably of diminished ecological relevance. These data reinforce the notion that <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> plays a unique role during initial infection while the antigenically variant <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content> proteins allow for persistence in the mammalian host.<\/jats:p>","DOI":"10.1111\/mmi.12286","type":"journal-article","created":{"date-parts":[[2013,6,10]],"date-time":"2013-06-10T08:21:30Z","timestamp":1370852490000},"page":"207-211","source":"Crossref","is-referenced-by-count":10,"title":["A call to order at the spirochaetal host\u2013pathogen interface"],"prefix":"10.1111","volume":"89","author":[{"given":"Wolfram R.","family":"Z\u00fcckert","sequence":"first","affiliation":[{"name":"Department of Microbiology, Molecular Genetics and Immunology University of Kansas School of Medicine  3901 Rainbow Boulevard Kansas City KS 66160 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