{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T03:34:16Z","timestamp":1773286456257,"version":"3.50.1"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            It has been demonstrated that\n            <jats:italic>Borrelia hermsii<\/jats:italic>\n            , a causative agent of relapsing fever, produces a factor H (FH) and FH-like protein 1 (FHL-1) binding protein. The binding protein has been designated FhbA. To determine if FH\/FHL-1 binding is widespread among\n            <jats:italic>B. hermsii<\/jats:italic>\n            isolates, a diverse panel of strains was tested for the FH\/FHL-1 binding phenotype and FhbA production. Most isolates (23\/24) produced FhbA and bound FH\/FHL-1. Potential variation in FhbA among isolates was analyzed by DNA sequence analyses. Two genetically distinct FhbA types, designated\n            <jats:italic>fhbA1<\/jats:italic>\n            and\n            <jats:italic>fhbA2<\/jats:italic>\n            , were delineated, and type-specific PCR primers were generated to allow for rapid differentiation. Pulsed-field gel electrophoresis and hybridization analyses demonstrated that all isolates that possess the gene carry it on a 200-kb linear plasmid (lp200), whereas isolates that lack the gene lack lp200 and instead carry an lp170. To determine if FhbA is antigenic during infection and to assess the specificity of the response, recombinant FhbA1 (rFhbA1) and rFhbA2 were screened with serum from infected mice and humans. FhbA was found to be expressed and antigenic and to elicit a potentially type-specific FhbA response. To localize the epitopes of FhbA1 and FhbA2, truncations were generated and screened with infection serum. The epitopes were determined to be conformationally defined. Collectively, these analyses indicate that FH\/FHL-1 binding is a widespread virulence mechanism for\n            <jats:italic>B. hermsii<\/jats:italic>\n            and provide insight into the genetic and antigenic structure of FhbA. The data also have potential implications for understanding the epidemiology of relapsing fever in North America and can be applied to the future development of species-specific diagnostic tools.\n          <\/jats:p>","DOI":"10.1128\/iai.00377-06","type":"journal-article","created":{"date-parts":[[2006,7,22]],"date-time":"2006-07-22T00:24:50Z","timestamp":1153527890000},"page":"4519-4529","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Immunological and Molecular Analyses of the\n            <i>Borrelia hermsii<\/i>\n            Factor H and Factor H-Like Protein 1 Binding Protein, FhbA: Demonstration of Its Utility as a Diagnostic Marker and Epidemiological Tool for Tick-Borne Relapsing Fever"],"prefix":"10.1128","volume":"74","author":[{"given":"Kelley M.","family":"Hovis","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin E.","family":"Schriefer","sequence":"additional","affiliation":[{"name":"Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sonia","family":"Bahlani","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard T.","family":"Marconi","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology"},{"name":"Center for the Study of Biological Complexity, Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia 23298-0678"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.7.3847"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2003-02-0426"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.36.12.3505-3508.1998"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/mr.50.4.381-400.1986"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a112406"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.66.2.815-819.1998"},{"key":"e_1_3_2_8_2","first-page":"542","volume":"69","year":"2003","unstructured":"Cutler, S., and A. 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