{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T07:19:15Z","timestamp":1791098355982,"version":"4.1.0"},"reference-count":46,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2011,2,1]],"date-time":"2011-02-01T00:00:00Z","timestamp":1296518400000},"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":[[2011,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Yersinia<\/jats:italic>\n            <jats:italic>pestis<\/jats:italic>\n            is a highly pathogenic Gram-negative organism and the causative agent of bubonic and pneumonic plague.\n            <jats:italic>Y<\/jats:italic>\n            .\n            <jats:italic>pestis<\/jats:italic>\n            is capable of causing major epidemics; thus, there is a need for vaccine targets and a greater understanding of the role of these targets in pathogenesis. Two prime\n            <jats:italic>Y<\/jats:italic>\n            .\n            <jats:italic>pestis<\/jats:italic>\n            vaccine candidates are the usher-chaperone fimbriae Psa and Caf. Herein we report that\n            <jats:italic>Y<\/jats:italic>\n            .\n            <jats:italic>pestis<\/jats:italic>\n            requires, in a nonredundant manner, both PsaA and Caf1 to achieve its full pathogenic ability in both pneumonic and bubonic plague in C57BL\/6J mice. Deletion of\n            <jats:italic>psaA<\/jats:italic>\n            leads to a decrease in the organ bacterial burden and to a significant increase in the 50% lethal dose (LD\n            <jats:sub>50<\/jats:sub>\n            ) after subcutaneous infection. Deletion of\n            <jats:italic>caf1<\/jats:italic>\n            also leads to a significant decrease in the organ bacterial burden but more importantly leads to a significantly greater increase in the LD\n            <jats:sub>50<\/jats:sub>\n            than was observed for the \u0394\n            <jats:italic>psaA<\/jats:italic>\n            mutant strain after subcutaneous infection of C57BL\/6J mice. Furthermore, the degree of attenuation of the \u0394\n            <jats:italic>caf1<\/jats:italic>\n            mutant strain is mouse background dependent, as the \u0394\n            <jats:italic>caf1<\/jats:italic>\n            mutant strain was attenuated to a lesser degree in BALB\/cJ mice by the subcutaneous route than in C57BL\/6J mice. This observation that the degree of requirement for Caf1 is dependent on the mouse background indicates that the virulence of\n            <jats:italic>Y<\/jats:italic>\n            .\n            <jats:italic>pestis<\/jats:italic>\n            is dependent on the genetic makeup of its host and provides further support for the hypothesis that PsaA and Caf1 have different targets.\n          <\/jats:p>","DOI":"10.1128\/iai.00981-10","type":"journal-article","created":{"date-parts":[[2010,11,30]],"date-time":"2010-11-30T05:12:27Z","timestamp":1291093947000},"page":"644-652","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":43,"title":["The Dependence of the\n            <i>Yersinia<\/i>\n            <i>pestis<\/i>\n            Capsule on Pathogenesis Is Influenced by the Mouse Background"],"prefix":"10.1128","volume":"79","author":[{"given":"Eric H.","family":"Weening","sequence":"first","affiliation":[{"name":"Department of Genetics, University of North Carolina, Chapel Hill, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason S.","family":"Cathelyn","sequence":"additional","affiliation":[{"name":"Division of Biology and Biomedical Sciences, Washington University, St. Louis, Missouri 63110"},{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Greer","family":"Kaufman","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew B.","family":"Lawrenz","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of North Carolina, Chapel Hill, North Carolina"},{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Price","sequence":"additional","affiliation":[{"name":"Division of Biology and Biomedical Sciences, Washington University, St. Louis, Missouri 63110"},{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William E.","family":"Goldman","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virginia L.","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Genetics, University of North Carolina, Chapel Hill, North Carolina"},{"name":"Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina"},{"name":"Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1099\/jmm.0.005678-0"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/1791246a0"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603456103"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2007.05907.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.72.6.851-857.1956"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.15.3.972-977.1977"},{"key":"e_1_3_2_8_2","first-page":"455","volume":"291","year":"2002","unstructured":"Cornelis, G. 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