{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T16:24:24Z","timestamp":1792599864279,"version":"4.5.0"},"reference-count":64,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2008,12,1]],"date-time":"2008-12-01T00:00:00Z","timestamp":1228089600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Several\n            <jats:italic>Borrelia burgdorferi<\/jats:italic>\n            genes induced under mammalian host conditions have been purported to be important in Lyme disease pathogenesis based on their binding to host structures. These genes include the\n            <jats:italic>dbpBA<\/jats:italic>\n            locus, whose products bind host decorin and glycosoaminoglycans. Recently, the\n            <jats:italic>dbpBA<\/jats:italic>\n            genes were reported to be involved in borrelial infectivity. Here we extended the previous observations by using culture and quantitative PCR to evaluate low- and high-dose murine infection by a \u0394\n            <jats:italic>dbpBA<\/jats:italic>\n            ::Gent\n            <jats:sup>r<\/jats:sup>\n            derivative of\n            <jats:italic>B. burgdorferi<\/jats:italic>\n            strain B31. The results indicate that the \u0394\n            <jats:italic>dbpBA<\/jats:italic>\n            ::Gent\n            <jats:sup>r<\/jats:sup>\n            mutant is attenuated in the ability to initially colonize and then persist in multiple tissues. The mutant exhibited a colonization defect as early as 3 days postinfection, before the development of an adaptive immune response, and after low-dose infection of SCID mice, which are deficient in adaptive immunity. These findings suggest that the inability to adhere to host decorin may promote clearance of\n            <jats:italic>B. burgdorferi<\/jats:italic>\n            , presumably via innate immune mechanisms. In a high-dose infection, the mutant disseminated to several tissues, particularly joint tissue, but it was generally cleared from these tissues by 3 weeks postinfection. Finally, following high-dose infection of SCID mice, the\n            <jats:italic>dbpBA<\/jats:italic>\n            mutant exhibited only a mild colonization defect, suggesting that the adaptive response is involved in the clearance of the mutant in immunocompetent mice. Taken together, these results suggest that the DbpBA proteins facilitate the colonization of multiple tissues by\n            <jats:italic>B. burgdorferi<\/jats:italic>\n            and are required for optimal resistance to both innate and adaptive immune mechanisms following needle inoculation.\n          <\/jats:p>","DOI":"10.1128\/iai.00690-08","type":"journal-article","created":{"date-parts":[[2008,9,23]],"date-time":"2008-09-23T00:25:42Z","timestamp":1222129542000},"page":"5694-5705","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":100,"title":["<i>Borrelia burgdorferi<\/i>\n            Lacking DbpBA Exhibits an Early Survival Defect during Experimental Infection"],"prefix":"10.1128","volume":"76","author":[{"given":"Eric H.","family":"Weening","sequence":"first","affiliation":[{"name":"Department of Microbial and Molecular 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