Essential role for OspA/B in the life cycle of the Lyme disease spirochete
The molecular basis of how Borrelia burgdorferi (Bb), the Lyme disease spirochete, maintains itself in nature via a complex life cycle in ticks and mammals is poorly understood. Outer surface (lipo)protein A (OspA) of Bb has been the most intensively studied of all borrelial molecular constituents,...
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| Veröffentlicht in: | The Journal of experimental medicine 2004-03, Vol.199 (5), p.641-648 |
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| container_title | The Journal of experimental medicine |
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| creator | Yang, Xiaofeng F Pal, Utpal Alani, Sophie M Fikrig, Erol Norgard, Michael V |
| description | The molecular basis of how Borrelia burgdorferi (Bb), the Lyme disease spirochete, maintains itself in nature via a complex life cycle in ticks and mammals is poorly understood. Outer surface (lipo)protein A (OspA) of Bb has been the most intensively studied of all borrelial molecular constituents, and hence, much has been speculated about the potential role(s) of OspA in the life cycle of Bb. However, the precise function of OspA (along with that of its close relative and operonic partner, outer surface [lipo]protein B [OspB]) heretofore has not been directly determined, due primarily to the inability to generate an OspA/B-deficient mutant from a virulent strain of Bb. In this study, we created an OspA/B-deficient mutant of an infectious human isolate of Bb (strain 297) and found that OspA/B function was not required for either Bb infection of mice or accompanying tissue pathology. However, OspA/B function was essential for Bb colonization of and survival within tick midguts, events crucial for sustaining Bb in its natural enzootic life cycle. |
| doi_str_mv | 10.1084/jem.20031960 |
| format | Article |
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Outer surface (lipo)protein A (OspA) of Bb has been the most intensively studied of all borrelial molecular constituents, and hence, much has been speculated about the potential role(s) of OspA in the life cycle of Bb. However, the precise function of OspA (along with that of its close relative and operonic partner, outer surface [lipo]protein B [OspB]) heretofore has not been directly determined, due primarily to the inability to generate an OspA/B-deficient mutant from a virulent strain of Bb. In this study, we created an OspA/B-deficient mutant of an infectious human isolate of Bb (strain 297) and found that OspA/B function was not required for either Bb infection of mice or accompanying tissue pathology. However, OspA/B function was essential for Bb colonization of and survival within tick midguts, events crucial for sustaining Bb in its natural enzootic life cycle.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20031960</identifier><identifier>PMID: 14981112</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Antigens, Bacterial - genetics ; Antigens, Bacterial - physiology ; Antigens, Surface - genetics ; Antigens, Surface - physiology ; Arthropod Vectors - microbiology ; Bacterial Outer Membrane Proteins - genetics ; Bacterial Outer Membrane Proteins - physiology ; Bacterial Vaccines ; Borrelia burgdorferi ; Borrelia burgdorferi - genetics ; Borrelia burgdorferi - growth & development ; Borrelia burgdorferi - physiology ; Gene Targeting ; Genes, Bacterial ; Humans ; Ixodes - microbiology ; Lipoproteins ; Lyme Disease - microbiology ; Lyme Disease - transmission ; Mutation ; Spirochetes ; Zoonoses - microbiology ; Zoonoses - transmission</subject><ispartof>The Journal of experimental medicine, 2004-03, Vol.199 (5), p.641-648</ispartof><rights>Copyright © 2004, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-627765156690ca161603ae589baab148e760c077af7870c1111e93e78495ec7c3</citedby><cites>FETCH-LOGICAL-c520t-627765156690ca161603ae589baab148e760c077af7870c1111e93e78495ec7c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14981112$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Xiaofeng F</creatorcontrib><creatorcontrib>Pal, Utpal</creatorcontrib><creatorcontrib>Alani, Sophie M</creatorcontrib><creatorcontrib>Fikrig, Erol</creatorcontrib><creatorcontrib>Norgard, Michael V</creatorcontrib><title>Essential role for OspA/B in the life cycle of the Lyme disease spirochete</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>The molecular basis of how Borrelia burgdorferi (Bb), the Lyme disease spirochete, maintains itself in nature via a complex life cycle in ticks and mammals is poorly understood. Outer surface (lipo)protein A (OspA) of Bb has been the most intensively studied of all borrelial molecular constituents, and hence, much has been speculated about the potential role(s) of OspA in the life cycle of Bb. However, the precise function of OspA (along with that of its close relative and operonic partner, outer surface [lipo]protein B [OspB]) heretofore has not been directly determined, due primarily to the inability to generate an OspA/B-deficient mutant from a virulent strain of Bb. In this study, we created an OspA/B-deficient mutant of an infectious human isolate of Bb (strain 297) and found that OspA/B function was not required for either Bb infection of mice or accompanying tissue pathology. However, OspA/B function was essential for Bb colonization of and survival within tick midguts, events crucial for sustaining Bb in its natural enzootic life cycle.</description><subject>Animals</subject><subject>Antigens, Bacterial - genetics</subject><subject>Antigens, Bacterial - physiology</subject><subject>Antigens, Surface - genetics</subject><subject>Antigens, Surface - physiology</subject><subject>Arthropod Vectors - microbiology</subject><subject>Bacterial Outer Membrane Proteins - genetics</subject><subject>Bacterial Outer Membrane Proteins - physiology</subject><subject>Bacterial Vaccines</subject><subject>Borrelia burgdorferi</subject><subject>Borrelia burgdorferi - genetics</subject><subject>Borrelia burgdorferi - growth & development</subject><subject>Borrelia burgdorferi - physiology</subject><subject>Gene Targeting</subject><subject>Genes, Bacterial</subject><subject>Humans</subject><subject>Ixodes - microbiology</subject><subject>Lipoproteins</subject><subject>Lyme Disease - microbiology</subject><subject>Lyme Disease - transmission</subject><subject>Mutation</subject><subject>Spirochetes</subject><subject>Zoonoses - microbiology</subject><subject>Zoonoses - transmission</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1PwzAQhi0EgvKxMSNPTATunMSOFySo-FSlLjBbrrlQo6QudorUf0-g5WtiOunu0av39DB2iHCKUBVnL9SeCoActYQNNsCygEyXebXJBgBCZAigdthuSi8AWBSl3GY7WOgKEcWA3V-lRLPO24bH0BCvQ-TjNL84u-R-xrsp8cbXxN3S9cdQf25Gy5b4k09kE_E09zG4KXW0z7Zq2yQ6WM899nh99TC8zUbjm7vhxShzpYAuk0IpWWIppQZnUaKE3FJZ6Ym1EywqUhIcKGVrVSlwfU0knZOqCl2SUy7fY-er3Pli0tKT6-tH25h59K2NSxOsN38vMz81z-HNCIG50EUfcLwOiOF1QakzrU-OmsbOKCySUSi10pX6F0SlRC4U9uDJCnQxpBSp_m6DYD4smd6S-bLU40e_P_iB11ryd-OpjDY</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Yang, Xiaofeng F</creator><creator>Pal, Utpal</creator><creator>Alani, Sophie M</creator><creator>Fikrig, Erol</creator><creator>Norgard, Michael V</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040301</creationdate><title>Essential role for OspA/B in the life cycle of the Lyme disease spirochete</title><author>Yang, Xiaofeng F ; Pal, Utpal ; Alani, Sophie M ; Fikrig, Erol ; Norgard, Michael V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c520t-627765156690ca161603ae589baab148e760c077af7870c1111e93e78495ec7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Antigens, Bacterial - genetics</topic><topic>Antigens, Bacterial - physiology</topic><topic>Antigens, Surface - genetics</topic><topic>Antigens, Surface - physiology</topic><topic>Arthropod Vectors - microbiology</topic><topic>Bacterial Outer Membrane Proteins - genetics</topic><topic>Bacterial Outer Membrane Proteins - physiology</topic><topic>Bacterial Vaccines</topic><topic>Borrelia burgdorferi</topic><topic>Borrelia burgdorferi - genetics</topic><topic>Borrelia burgdorferi - growth & development</topic><topic>Borrelia burgdorferi - physiology</topic><topic>Gene Targeting</topic><topic>Genes, Bacterial</topic><topic>Humans</topic><topic>Ixodes - microbiology</topic><topic>Lipoproteins</topic><topic>Lyme Disease - microbiology</topic><topic>Lyme Disease - transmission</topic><topic>Mutation</topic><topic>Spirochetes</topic><topic>Zoonoses - microbiology</topic><topic>Zoonoses - transmission</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Xiaofeng F</creatorcontrib><creatorcontrib>Pal, Utpal</creatorcontrib><creatorcontrib>Alani, Sophie M</creatorcontrib><creatorcontrib>Fikrig, Erol</creatorcontrib><creatorcontrib>Norgard, Michael V</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Xiaofeng F</au><au>Pal, Utpal</au><au>Alani, Sophie M</au><au>Fikrig, Erol</au><au>Norgard, Michael V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Essential role for OspA/B in the life cycle of the Lyme disease spirochete</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>199</volume><issue>5</issue><spage>641</spage><epage>648</epage><pages>641-648</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>The molecular basis of how Borrelia burgdorferi (Bb), the Lyme disease spirochete, maintains itself in nature via a complex life cycle in ticks and mammals is poorly understood. Outer surface (lipo)protein A (OspA) of Bb has been the most intensively studied of all borrelial molecular constituents, and hence, much has been speculated about the potential role(s) of OspA in the life cycle of Bb. However, the precise function of OspA (along with that of its close relative and operonic partner, outer surface [lipo]protein B [OspB]) heretofore has not been directly determined, due primarily to the inability to generate an OspA/B-deficient mutant from a virulent strain of Bb. In this study, we created an OspA/B-deficient mutant of an infectious human isolate of Bb (strain 297) and found that OspA/B function was not required for either Bb infection of mice or accompanying tissue pathology. However, OspA/B function was essential for Bb colonization of and survival within tick midguts, events crucial for sustaining Bb in its natural enzootic life cycle.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>14981112</pmid><doi>10.1084/jem.20031960</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens, Bacterial - genetics Antigens, Bacterial - physiology Antigens, Surface - genetics Antigens, Surface - physiology Arthropod Vectors - microbiology Bacterial Outer Membrane Proteins - genetics Bacterial Outer Membrane Proteins - physiology Bacterial Vaccines Borrelia burgdorferi Borrelia burgdorferi - genetics Borrelia burgdorferi - growth & development Borrelia burgdorferi - physiology Gene Targeting Genes, Bacterial Humans Ixodes - microbiology Lipoproteins Lyme Disease - microbiology Lyme Disease - transmission Mutation Spirochetes Zoonoses - microbiology Zoonoses - transmission |
| title | Essential role for OspA/B in the life cycle of the Lyme disease spirochete |
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