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These adaptations include shifting among the major outer surface lipoproteins <jats:styled-content style=\"fixed-case\">OspA<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content> at different stages of the infectious cycle. We hypothesize that these proteins carry out a basic but essential function, and that <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content> fulfil this requirement during early and persistent stages of mammalian infection respectively. Previous work by other investigators suggested that several <jats:italic><jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>.\u2009burgdorferi<\/jats:italic> lipoproteins, including <jats:styled-content style=\"fixed-case\">OspA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content>, could substitute for <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> at the initial stage of mouse infection, when <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> is transiently but absolutely required. In this study, we assessed whether <jats:styled-content style=\"fixed-case\"><jats:italic>vlsE<\/jats:italic><\/jats:styled-content> and <jats:styled-content style=\"fixed-case\"><jats:italic>ospA<\/jats:italic><\/jats:styled-content> could restore infectivity to an <jats:styled-content style=\"fixed-case\"><jats:italic>ospC<\/jats:italic><\/jats:styled-content> mutant, and found that neither gene product effectively compensated for the absence of <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> during early infection. In contrast, we determined that <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> production was required by <jats:italic><jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>.\u2009burgdorferi<\/jats:italic> throughout <jats:styled-content style=\"fixed-case\">SCID<\/jats:styled-content> mouse infection if the <jats:styled-content style=\"fixed-case\"><jats:italic>vlsE<\/jats:italic><\/jats:styled-content> gene were absent. Together, these results indicate that <jats:styled-content style=\"fixed-case\">OspC<\/jats:styled-content> can substitute for <jats:styled-content style=\"fixed-case\">VlsE<\/jats:styled-content> when antigenic variation is unnecessary, but that these two abundant lipoproteins are optimized for their related but specific roles during early and persistent mammalian infection by <jats:italic><jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>.\u2009burgdorferi<\/jats:italic>.<\/jats:p>","DOI":"10.1111\/mmi.12271","type":"journal-article","created":{"date-parts":[[2013,5,22]],"date-time":"2013-05-22T07:19:51Z","timestamp":1369207191000},"page":"216-227","source":"Crossref","is-referenced-by-count":60,"title":["Lipoprotein succession in <i><scp>B<\/scp>orrelia burgdorferi<\/i>: similar but distinct roles for <scp>OspC<\/scp> and <scp>VlsE<\/scp> at different stages of mammalian 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