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As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type\n            <jats:italic>revA<\/jats:italic>\n            gene restored heart infectivity to wild-type levels. Additionally,\n            <jats:italic>revA<\/jats:italic>\n            mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while\n            <jats:italic>revA<\/jats:italic>\n            is not absolutely essential for infection, deletion of\n            <jats:italic>revA<\/jats:italic>\n            had distinct effects on dissemination, arthritis severity, and host response.\n          <\/jats:p>","DOI":"10.1128\/iai.00530-15","type":"journal-article","created":{"date-parts":[[2015,7,7]],"date-time":"2015-07-07T02:30:36Z","timestamp":1436236236000},"page":"3675-3683","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":23,"title":["Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease"],"prefix":"10.1128","volume":"83","author":[{"given":"Rebecca","family":"Byram","sequence":"first","affiliation":[{"name":"Division of Vector-Borne Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert A.","family":"Gaultney","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angela M.","family":"Floden","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Hellekson","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandee L.","family":"Stone","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy","family":"Bowman","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky School of Medicine, Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Stevenson","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky School of Medicine, Lexington, Kentucky, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara J. 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