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Proteins that mediate critical interactions with the host during invasive disease are likely to be secreted. Many secreted proteins require addition of disulfide bonds by the DsbA disulfide oxidoreductase for activity or stability. In this study, we evaluated the role in\n            <jats:italic>H. influenzae<\/jats:italic>\n            pathogenesis of DsbA, as well as HbpA, a substrate of DsbA. Mutants of\n            <jats:italic>H. influenzae<\/jats:italic>\n            Rd and type b strain Eagan having nonpolar deletions of\n            <jats:italic>dsbA<\/jats:italic>\n            were attenuated for bacteremia in animal models, and complemented strains exhibited virulence equivalent to that of the parental strains. Comparison of predicted secreted proteins in\n            <jats:italic>H. influenzae<\/jats:italic>\n            to known DsbA substrates in other species revealed several proteins that could contribute to the role of\n            <jats:italic>dsbA<\/jats:italic>\n            in virulence. One candidate, the heme transport protein, HbpA, was examined because of the importance of exogenous heme for aerobic growth of\n            <jats:italic>H. influenzae<\/jats:italic>\n            . The presence of a\n            <jats:italic>dsbA<\/jats:italic>\n            -dependent disulfide bond in HbpA was verified by an alkylation protection assay, and HbpA was less abundant in a\n            <jats:italic>dsbA<\/jats:italic>\n            mutant. The\n            <jats:italic>hbpA<\/jats:italic>\n            mutant exhibited reduced bacteremia in the mouse model, and complementation restored its in vivo phenotype to that of the parental strain. These results indicate that\n            <jats:italic>dsbA<\/jats:italic>\n            is required in vivo and that HbpA and additional DsbA-dependent factors are likely to participate in\n            <jats:italic>H. influenzae<\/jats:italic>\n            pathogenesis.\n          <\/jats:p>","DOI":"10.1128\/iai.01378-07","type":"journal-article","created":{"date-parts":[[2008,1,23]],"date-time":"2008-01-23T01:44:47Z","timestamp":1201052687000},"page":"1498-1508","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":24,"title":["The Periplasmic Disulfide Oxidoreductase DsbA Contributes to\n            <i>Haemophilus influenzae<\/i>\n            Pathogenesis"],"prefix":"10.1128","volume":"76","author":[{"given":"Charles V.","family":"Rosadini","sequence":"first","affiliation":[{"name":"Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandy M. 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