The Borrelia hermsii factor H binding protein FhbA is not required for infectivity in mice or for resistance to human complement in vitro
The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii. It has been hypothesized that B. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement. In vitro, B. hermsii produces a single FH binding...
Saved in:
Published in | Infection and immunity Vol. 82; no. 8; pp. 3324 - 3332 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Society for Microbiology
01.08.2014
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii. It has been hypothesized that B. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement. In vitro, B. hermsii produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen for B. hermsii infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factor in vivo has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated a B. hermsii fhbA deletion mutant (the B. hermsii YORΔfhbA strain) through allelic exchange mutagenesis. Deletion of fhbA abolished FH binding by the YORΔfhbA strain and eliminated cleavage of C3b on the cell surface. However, the YORΔfhbA strain remained infectious in mice and retained resistance to killing in vitro by human complement. Collectively, these results indicate that B. hermsii employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice. |
---|---|
AbstractList | The primary causative agent of tick-borne relapsing fever in North America is
Borrelia hermsii
. It has been hypothesized that
B. hermsii
evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement.
In vitro
,
B. hermsii
produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen for
B. hermsii
infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factor
in vivo
has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated a
B. hermsii
fhbA
deletion mutant (the
B. hermsii
YORΔ
fhbA
strain) through allelic exchange mutagenesis. Deletion of
fhbA
abolished FH binding by the YORΔ
fhbA
strain and eliminated cleavage of C3b on the cell surface. However, the YORΔ
fhbA
strain remained infectious in mice and retained resistance to killing
in vitro
by human complement. Collectively, these results indicate that
B. hermsii
employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice. The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii. It has been hypothesized that B. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement. In vitro, B. hermsii produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen for B. hermsii infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factor in vivo has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated a B. hermsii fhbA deletion mutant (the B. hermsii YOR Delta fhbA strain) through allelic exchange mutagenesis. Deletion of fhbA abolished FH binding by the YOR Delta fhbA strain and eliminated cleavage of C3b on the cell surface. However, the YOR Delta fhbA strain remained infectious in mice and retained resistance to killing in vitro by human complement. Collectively, these results indicate that B. hermsii employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice. ABSTRACT The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii . It has been hypothesized that B. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement. In vitro , B. hermsii produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen for B. hermsii infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factor in vivo has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated a B. hermsii fhbA deletion mutant (the B. hermsii YORΔ fhbA strain) through allelic exchange mutagenesis. Deletion of fhbA abolished FH binding by the YORΔ fhbA strain and eliminated cleavage of C3b on the cell surface. However, the YORΔ fhbA strain remained infectious in mice and retained resistance to killing in vitro by human complement. Collectively, these results indicate that B. hermsii employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice. The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii. It has been hypothesized that B. hermsii evades complement-mediated destruction by binding factor H (FH), a host-derived negative regulator of complement. In vitro, B. hermsii produces a single FH binding protein designated FhbA (FH binding protein A). The properties and ligand binding activity of FhbA suggest that it plays multiple roles in pathogenesis. It binds plasminogen and has been identified as a significant target of a B1b B cell-mediated IgM response in mice. FhbA has also been explored as a potential diagnostic antigen for B. hermsii infection in humans. The ability to test the hypothesis that FhbA is a critical virulence factor in vivo has been hampered by the lack of well-developed systems for the genetic manipulation of the relapsing fever spirochetes. In this report, we have successfully generated a B. hermsii fhbA deletion mutant (the B. hermsii YORΔfhbA strain) through allelic exchange mutagenesis. Deletion of fhbA abolished FH binding by the YORΔfhbA strain and eliminated cleavage of C3b on the cell surface. However, the YORΔfhbA strain remained infectious in mice and retained resistance to killing in vitro by human complement. Collectively, these results indicate that B. hermsii employs an FhbA/FH-independent mechanism of complement evasion that allows for resistance to killing by human complement and persistence in mice. |
Author | Marconi, Richard T Tegels, Brittney K Mallory, Katherine L Earnhart, Christopher G Miller, Daniel P Fine, Lindy M |
Author_xml | – sequence: 1 givenname: Lindy M surname: Fine fullname: Fine, Lindy M organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA – sequence: 2 givenname: Daniel P surname: Miller fullname: Miller, Daniel P organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA – sequence: 3 givenname: Katherine L surname: Mallory fullname: Mallory, Katherine L organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA – sequence: 4 givenname: Brittney K surname: Tegels fullname: Tegels, Brittney K organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA – sequence: 5 givenname: Christopher G surname: Earnhart fullname: Earnhart, Christopher G organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA – sequence: 6 givenname: Richard T surname: Marconi fullname: Marconi, Richard T email: rmarconi@vcu.edu organization: Department of Microbiology and Immunology, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA Center for the Study of Biological Complexity, Virginia Commonwealth University Medical Center, Richmond, Virginia, USA rmarconi@vcu.edu |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24866803$$D View this record in MEDLINE/PubMed |
BookMark | eNpVkU1v3CAQhlGVqtmkvfVcceyhTvkyxpdKm6hpVorUS3pGGA8xlQ0bwJHyE_qvyzZplEggYOaZl4H3BB2FGAChj5ScUcrU1912d0ao6llDxRu0oaRXTdsydoQ2hNC-6VvZHaOTnH_XoxBCvUPHTCgpFeEb9OdmAnweU4LZGzxBWrL32BlbYsJXePBh9OEW71Ms4AO-nIYt9hmHWHCCu9UnGLGrqA8ObPH3vjzUPV68BVzDh1SC7HMxoUZKxNO6mIBtXPYzLBDKga5VKb5Hb52ZM3x4Wk_Rr8vvNxdXzfXPH7uL7XVjhSSl6YZBctIxWd9opOhGN3KhutbQXlLlut4qSTgHxQYgLa8T-joEc844BpKfom-Puvt1WGC0tYdkZr1PfjHpQUfj9etM8JO-jfdaUC4ZYVXg85NAincr5KIXny3MswkQ16xpK-tHU961Ff3yiNoUc07gnq-hRB_c09U9_c89TUXFP71s7Rn-bxf_C9yxmR8 |
CitedBy_id | crossref_primary_10_3389_fcimb_2019_00290 crossref_primary_10_3389_fimmu_2020_01560 crossref_primary_10_3389_fimmu_2021_602277 crossref_primary_10_1093_jme_tjw171 crossref_primary_10_1371_journal_ppat_1010338 crossref_primary_10_3109_1040841X_2014_972336 crossref_primary_10_3389_fimmu_2017_00571 crossref_primary_10_3389_fimmu_2017_00012 crossref_primary_10_3389_fmicb_2017_00328 crossref_primary_10_1371_journal_pone_0147707 |
Cites_doi | 10.3201/eid1507.090223 10.1371/journal.ppat.1003308 10.1128/IAI.69.1.446-455.2001 10.1016/S1567-5769(00)00041-2 10.1128/IAI.69.9.5832-5839.2001 10.4269/ajtmh.2002.66.753 10.1086/516273 10.3201/eid1303.060958 10.1007/978-1-4614-5404-5_3 10.1128/IAI.71.6.3597-3602.2003 10.1016/j.imlet.2009.07.005 10.1016/j.molimm.2010.05.007 10.1074/jbc.M007994200 10.1128/IAI.74.5.3030-3034.2006 10.1016/j.molimm.2008.06.028 10.1128/iai.63.7.2478-2484.1995 10.1128/JB.05037-11 10.1128/JB.180.18.4974-4981.1998 10.1002/eji.200323571 10.1074/jbc.M111.323287 10.1128/JCM.41.8.3905-3910.2003 10.1042/bst0300971 10.1016/S0092-8674(00)80298-6 10.1128/JCM.39.7.2500-2507.2001 10.1128/jcm.33.9.2427-2434.1995 10.1016/S0140-6736(06)68968-X 10.1128/IAI.00377-06 10.1128/IAI.69.12.7800-7809.2001 10.1128/IAI.01266-07 10.1371/journal.pntd.0000698 10.1128/IAI.01544-08 10.1086/516276 10.1128/JB.186.9.2612-2618.2004 10.1128/IAI.74.4.2007-2014.2006 10.3109/00016349709024361 10.4049/jimmunol.178.11.7292 10.3201/eid0909.030280 10.4161/hv.4661 10.1128/mr.50.4.381-400.1986 10.1086/514496 10.1128/IAI.00007-06 10.1016/j.vaccine.2008.11.015 10.1111/j.1365-2958.2006.05122.x |
ContentType | Journal Article |
Copyright | Copyright © 2014, American Society for Microbiology. All Rights Reserved. Copyright © 2014, American Society for Microbiology. All Rights Reserved. 2014 American Society for Microbiology |
Copyright_xml | – notice: Copyright © 2014, American Society for Microbiology. All Rights Reserved. – notice: Copyright © 2014, American Society for Microbiology. All Rights Reserved. 2014 American Society for Microbiology |
DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 7QL 7T5 C1K H94 5PM |
DOI | 10.1128/IAI.01892-14 |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef Bacteriology Abstracts (Microbiology B) Immunology Abstracts Environmental Sciences and Pollution Management AIDS and Cancer Research Abstracts PubMed Central (Full Participant titles) |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef AIDS and Cancer Research Abstracts Immunology Abstracts Bacteriology Abstracts (Microbiology B) Environmental Sciences and Pollution Management |
DatabaseTitleList | AIDS and Cancer Research Abstracts CrossRef MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Biology |
EISSN | 1098-5522 |
Editor | Blanke, S. R. |
Editor_xml | – sequence: 1 givenname: S. R. surname: Blanke fullname: Blanke, S. R. |
EndPage | 3332 |
ExternalDocumentID | 10_1128_IAI_01892_14 24866803 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NIDCR NIH HHS grantid: F31 DE023000 – fundername: NIDCR NIH HHS grantid: F31-DE023000 – fundername: NIDCR NIH HHS grantid: R01-DE017401 – fundername: NIAID NIH HHS grantid: R01 AI037787 – fundername: NCATS NIH HHS grantid: UL1 TR000058 – fundername: NCATS NIH HHS grantid: UL1TR000058 – fundername: NIAID NIH HHS grantid: R01-AI037787 – fundername: NIDCR NIH HHS grantid: R01 DE017401 |
GroupedDBID | --- -DZ -~X .55 .GJ 0R~ 18M 29I 2WC 39C 3O- 4.4 41~ 53G 5GY 5RE 5VS 85S ABOCM ACGFO ADBBV AENEX AGCDD AGVNZ AI. ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BTFSW C1A CGR CS3 CUY CVF D0S DIK DU5 E3Z EBS ECM EIF EJD F5P FRP GX1 H13 HYE HZ~ H~9 IH2 J5H KQ8 L7B MVM NEJ NPM O9- OHT OK1 P2P RHF RHI RNS RPM RSF SJN TR2 TWZ UCJ UPT VH1 VQA W2D W8F WH7 WHG WOQ X7M Y6R ZGI ZXP ~KM AAYXX CITATION 7QL 7T5 C1K H94 5PM |
ID | FETCH-LOGICAL-c460t-7bb630726552a647dfd34875a19618f79c86033e82be053e05e95e942ffaf2e63 |
IEDL.DBID | RPM |
ISSN | 0019-9567 |
IngestDate | Tue Sep 17 21:08:48 EDT 2024 Wed Jul 24 15:15:29 EDT 2024 Thu Sep 12 20:08:51 EDT 2024 Sat Sep 28 07:54:05 EDT 2024 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 8 |
Language | English |
License | Copyright © 2014, American Society for Microbiology. All Rights Reserved. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c460t-7bb630726552a647dfd34875a19618f79c86033e82be053e05e95e942ffaf2e63 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Present address: Lindy M. Fine, University of Maryland Center for Environmental Science, Cambridge, Maryland, USA. |
OpenAccessLink | https://iai.asm.org/content/iai/82/8/3324.full.pdf |
PMID | 24866803 |
PQID | 1560141375 |
PQPubID | 23462 |
PageCount | 9 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_4136202 proquest_miscellaneous_1560141375 crossref_primary_10_1128_IAI_01892_14 pubmed_primary_24866803 |
PublicationCentury | 2000 |
PublicationDate | 2014-08-01 |
PublicationDateYYYYMMDD | 2014-08-01 |
PublicationDate_xml | – month: 08 year: 2014 text: 2014-08-01 day: 01 |
PublicationDecade | 2010 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States – name: 1752 N St., N.W., Washington, DC |
PublicationTitle | Infection and immunity |
PublicationTitleAlternate | Infect Immun |
PublicationYear | 2014 |
Publisher | American Society for Microbiology |
Publisher_xml | – name: American Society for Microbiology |
References | 21551306 - J Bacteriol. 2011 Jul;193(13):3241-5 9455525 - Clin Infect Dis. 1998 Jan;26(1):151-64 17513779 - J Immunol. 2007 Jun 1;178(11):7292-301 18674818 - Mol Immunol. 2008 Oct;45(16):4057-63 20532227 - PLoS Negl Trop Dis. 2010;4(6):e698 5813010 - J Immunol. 1969 Mar;102(3):533-43 16861638 - Infect Immun. 2006 Aug;74(8):4519-29 7494041 - J Clin Microbiol. 1995 Sep;33(9):2427-34 19388168 - Vaccine. 2008 Dec 30;26 Suppl 8:I67-74 3540570 - Microbiol Rev. 1986 Dec;50(4):381-400 12616490 - Eur J Immunol. 2003 Mar;33(3):697-707 9455520 - Clin Infect Dis. 1998 Jan;26(1):122-31 17552097 - Emerg Infect Dis. 2007 Mar;13(3):436-42 20580090 - Mol Immunol. 2010 Aug;47(13):2187-97 16815378 - Lancet. 2006 Jul 1;368(9529):37-43 11113124 - J Biol Chem. 2001 Mar 16;276(11):8427-35 12440956 - Biochem Soc Trans. 2002 Nov;30(Pt 6):971-8 15090501 - J Bacteriol. 2004 May;186(9):2612-8 9351408 - Acta Obstet Gynecol Scand. 1997 Oct;76(9):834-8 23637600 - PLoS Pathog. 2013;9(4):e1003308 16790790 - Infect Immun. 2006 Jul;74(7):4157-63 12904415 - J Clin Microbiol. 2003 Aug;41(8):3905-10 9215633 - Cell. 1997 Jun 27;89(7):1111-9 9733706 - J Bacteriol. 1998 Sep;180(18):4974-81 7790059 - Infect Immun. 1995 Jul;63(7):2478-84 9243047 - Clin Infect Dis. 1997 Jul;25(1):139-44 22451663 - J Biol Chem. 2012 May 25;287(22):18831-42 11500461 - Infect Immun. 2001 Sep;69(9):5832-9 19616581 - Immunol Lett. 2009 Sep 22;126(1-2):1-7 12761145 - Infect Immun. 2003 Jun;71(6):3597-602 16622245 - Infect Immun. 2006 May;74(5):3030-4 19204088 - Infect Immun. 2009 Apr;77(4):1417-25 19624916 - Emerg Infect Dis. 2009 Jul;15(7):1026-31 18299341 - Infect Immun. 2008 May;76(5):2113-22 11367524 - Int Immunopharmacol. 2001 Mar;1(3):393-401 16552029 - Infect Immun. 2006 Apr;74(4):2007-14 16629672 - Mol Microbiol. 2006 May;60(3):710-22 17921702 - Hum Vaccin. 2007 Nov-Dec;3(6):281-9 11427560 - J Clin Microbiol. 2001 Jul;39(7):2500-7 12224586 - Am J Trop Med Hyg. 2002 Jun;66(6):753-8 14519254 - Emerg Infect Dis. 2003 Sep;9(9):1151-4 4999095 - J Immunol. 1971 Sep;107(3):742-50 11119536 - Infect Immun. 2001 Jan;69(1):446-55 11705962 - Infect Immun. 2001 Dec;69(12):7800-9 e_1_3_2_26_2 e_1_3_2_27_2 e_1_3_2_48_2 e_1_3_2_28_2 e_1_3_2_29_2 e_1_3_2_41_2 e_1_3_2_40_2 e_1_3_2_20_2 e_1_3_2_43_2 e_1_3_2_21_2 e_1_3_2_42_2 e_1_3_2_22_2 e_1_3_2_45_2 e_1_3_2_23_2 e_1_3_2_44_2 e_1_3_2_24_2 e_1_3_2_47_2 e_1_3_2_25_2 e_1_3_2_46_2 Felsenfeld O (e_1_3_2_12_2) 1971 McDowell JV (e_1_3_2_14_2) 2012 e_1_3_2_9_2 e_1_3_2_15_2 e_1_3_2_38_2 e_1_3_2_8_2 e_1_3_2_16_2 e_1_3_2_37_2 e_1_3_2_7_2 e_1_3_2_6_2 e_1_3_2_39_2 e_1_3_2_19_2 e_1_3_2_30_2 e_1_3_2_32_2 e_1_3_2_10_2 e_1_3_2_31_2 e_1_3_2_5_2 e_1_3_2_11_2 e_1_3_2_34_2 e_1_3_2_4_2 e_1_3_2_33_2 e_1_3_2_13_2 e_1_3_2_36_2 e_1_3_2_2_2 e_1_3_2_35_2 Cutler S (e_1_3_2_3_2) 2003; 69 Ruddy S (e_1_3_2_18_2) 1971; 107 Ruddy S (e_1_3_2_17_2) 1969; 102 |
References_xml | – ident: e_1_3_2_11_2 doi: 10.3201/eid1507.090223 – ident: e_1_3_2_31_2 doi: 10.1371/journal.ppat.1003308 – ident: e_1_3_2_39_2 doi: 10.1128/IAI.69.1.446-455.2001 – ident: e_1_3_2_29_2 doi: 10.1016/S1567-5769(00)00041-2 – ident: e_1_3_2_41_2 doi: 10.1128/IAI.69.9.5832-5839.2001 – ident: e_1_3_2_7_2 doi: 10.4269/ajtmh.2002.66.753 – ident: e_1_3_2_8_2 doi: 10.1086/516273 – ident: e_1_3_2_10_2 doi: 10.3201/eid1303.060958 – start-page: 43 volume-title: The pathogenic spirochetes: strategies for evasion of host immunity and persistence year: 2012 ident: e_1_3_2_14_2 doi: 10.1007/978-1-4614-5404-5_3 contributor: fullname: McDowell JV – ident: e_1_3_2_24_2 doi: 10.1128/IAI.71.6.3597-3602.2003 – ident: e_1_3_2_32_2 doi: 10.1016/j.imlet.2009.07.005 – ident: e_1_3_2_16_2 doi: 10.1016/j.molimm.2010.05.007 – volume: 69 start-page: 542 year: 2003 ident: e_1_3_2_3_2 article-title: Tick-borne relapsing fever in Tanzania—a forgotten problem? publication-title: ASM News contributor: fullname: Cutler S – volume-title: Warren H. Green, Inc. year: 1971 ident: e_1_3_2_12_2 contributor: fullname: Felsenfeld O – volume: 102 start-page: 533 year: 1969 ident: e_1_3_2_17_2 article-title: C3 inactivator of man. I. Hemolytic measurement by the inactivation of cell-bound C3 publication-title: J. Immunol. contributor: fullname: Ruddy S – ident: e_1_3_2_21_2 doi: 10.1074/jbc.M007994200 – ident: e_1_3_2_48_2 doi: 10.1128/IAI.74.5.3030-3034.2006 – ident: e_1_3_2_45_2 doi: 10.1016/j.molimm.2008.06.028 – ident: e_1_3_2_46_2 doi: 10.1128/iai.63.7.2478-2484.1995 – volume: 107 start-page: 742 year: 1971 ident: e_1_3_2_18_2 article-title: C3b inactivator of man. II. Fragments produced by C3b inactivator cleavage of cell-bound or fluid phase C3b publication-title: J. Immunol. contributor: fullname: Ruddy S – ident: e_1_3_2_34_2 doi: 10.1128/JB.05037-11 – ident: e_1_3_2_37_2 doi: 10.1128/JB.180.18.4974-4981.1998 – ident: e_1_3_2_22_2 doi: 10.1002/eji.200323571 – ident: e_1_3_2_47_2 doi: 10.1074/jbc.M111.323287 – ident: e_1_3_2_28_2 doi: 10.1128/JCM.41.8.3905-3910.2003 – ident: e_1_3_2_33_2 doi: 10.1042/bst0300971 – ident: e_1_3_2_40_2 doi: 10.1016/S0092-8674(00)80298-6 – ident: e_1_3_2_35_2 doi: 10.1128/JCM.39.7.2500-2507.2001 – ident: e_1_3_2_36_2 doi: 10.1128/jcm.33.9.2427-2434.1995 – ident: e_1_3_2_6_2 doi: 10.1016/S0140-6736(06)68968-X – ident: e_1_3_2_26_2 doi: 10.1128/IAI.00377-06 – ident: e_1_3_2_23_2 doi: 10.1128/IAI.69.12.7800-7809.2001 – ident: e_1_3_2_27_2 doi: 10.1128/IAI.01266-07 – ident: e_1_3_2_43_2 doi: 10.1371/journal.pntd.0000698 – ident: e_1_3_2_30_2 doi: 10.1128/IAI.01544-08 – ident: e_1_3_2_13_2 doi: 10.1086/516276 – ident: e_1_3_2_19_2 doi: 10.1128/JB.186.9.2612-2618.2004 – ident: e_1_3_2_25_2 doi: 10.1128/IAI.74.4.2007-2014.2006 – ident: e_1_3_2_5_2 doi: 10.3109/00016349709024361 – ident: e_1_3_2_20_2 doi: 10.4049/jimmunol.178.11.7292 – ident: e_1_3_2_9_2 doi: 10.3201/eid0909.030280 – ident: e_1_3_2_38_2 doi: 10.4161/hv.4661 – ident: e_1_3_2_2_2 doi: 10.1128/mr.50.4.381-400.1986 – ident: e_1_3_2_4_2 doi: 10.1086/514496 – ident: e_1_3_2_44_2 doi: 10.1128/IAI.00007-06 – ident: e_1_3_2_15_2 doi: 10.1016/j.vaccine.2008.11.015 – ident: e_1_3_2_42_2 doi: 10.1111/j.1365-2958.2006.05122.x |
SSID | ssj0014448 |
Score | 2.2572005 |
Snippet | The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii. It has been hypothesized that B. hermsii evades... ABSTRACT The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii . It has been hypothesized that B. hermsii evades... The primary causative agent of tick-borne relapsing fever in North America is Borrelia hermsii . It has been hypothesized that B. hermsii evades... |
SourceID | pubmedcentral proquest crossref pubmed |
SourceType | Open Access Repository Aggregation Database Index Database |
StartPage | 3324 |
SubjectTerms | Animals Blood Bactericidal Activity Borrelia - genetics Borrelia - immunology Borrelia hermsii Carrier Proteins - genetics Carrier Proteins - metabolism Complement System Proteins - immunology Disease Models, Animal Gene Deletion Humans Mice Molecular Pathogenesis Relapsing Fever - immunology Relapsing Fever - microbiology Virulence Factors - genetics Virulence Factors - metabolism |
Title | The Borrelia hermsii factor H binding protein FhbA is not required for infectivity in mice or for resistance to human complement in vitro |
URI | https://www.ncbi.nlm.nih.gov/pubmed/24866803 https://search.proquest.com/docview/1560141375 https://pubmed.ncbi.nlm.nih.gov/PMC4136202 |
Volume | 82 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Na9wwEB2ygZZeSpp-ZJs0TKE9encty5J83IQuuy0b0tCU3IxkycSQtUPWOfQn9F9nJNuhaW8F-2JJxnhG0hvmaR7AJ-ZiabmmmRY7G3Gb6EjPUh0VqXQp5yZVHcv3TCwv-der9GoH0uEsTCDtF6aa1DebSV1dB27l7aaYDjyx6fn6lBZeQUH7dAQjmSRDiN6nDjjn_fKbRQT-5cB2Z2q6mq8ms1hlLIq9Hg_jSgg1yGUNW9I_OPNvuuQf-89iD172wBHn3Qe-gh1X78OzTkry1z48X_dJ8tfwm0yPJ15146bSSDbZbKsKF0FYB5d4UoWDLHjuKzRUNS6uzRxXWzxrWrxwnhjsLBKUxVXH0_LiEkj91rSkID32TRdu63EnOQy2DYZEAPqVpeOi00j8WbV3zRu4XHz5cbqMesWFqOBi1kbSGEGTnok0ZVpwaUub-IhGx14YppRZocQsSZxixktK0O0yujgrS10yJ5K3sFs3tTsAJBxkRMl4IcuYW6uNYrI0NsksYcQsK8bwefjp-W1XWCMPAQlTOdkpD3aiwGQMHweL5OT5Pp2ha9fcb3N_BjwmV5DpGN51Fnp802DaMcgntnvs4KtqP20hZwvVtXvnev_fIw_hBaEq3rEEj2C3vbt3Hwi5tOYYRt--q-Pgrw-0Y-2o |
link.rule.ids | 230,315,733,786,790,891,27955,27956,53825,53827 |
linkProvider | National Library of Medicine |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb5wwEB6lqfq49JG2yfbpSu0RdjF-wHETdbW02VUUJVFuyMZGQc1ClGUP7T_ov-4YcNSkp1aCC7YRaMbjb-TP8wF8ojaShimcaZE1ATOxCtSEq6Dg0nLGNE96lu9SzE_Z13N-vgXcn4XpSPuFrsL6chXW1UXHrbxaFWPPExsfLQ4w8ApM2sf34D7OV8p9kj5sHjDGhgCcBgj_pee702ScTbNwEiUpDSKnyENZIkTiBbP8ovQX0rxLmPxjBZo9hTP_7T3x5Hu4aXVY_LxT1vGff-4ZPBkwKZn2zc9hy9Y78KBXqfyxAw8Xw_77C_iFXkX2naDHZaUImnu1rioy6zR7yJzsV90ZGXLkij9UNZld6CnJ1mTZtOTYOs6xNQRRMsl6CpjTrSDYb4HRiuBj13Rs1w7Soi-StiHdHgNxQaunueNIcla1181LOJ19OTmYB4OYQ1AwMWkDqbXAeEIF51QJJk1pYpcsqchpzpQyLRIxiWObUO3UKvC2KV6MlqUqqRXxK9ium9ruAUGIpUVJWSHLiBmjdEJlqU2cGoSfaVqM4LO3Zn7V1-zIu1yHJjk6QN45AOY8I_joTZ3jpHI7Jaq2zWadu-PlERpC8hHs9qa_eZP3mRHIW05x08EV7L7dgqbuCncPpn393yM_wKP5yeIwP8yW397AYwRvrCcjvoXt9npj3yFAavX7bjr8BqM_Dqo |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELagiIpLC4XCUgqDBMckG8exk-O2NNoAu1pVFFVcIjt21IhusupmD-Uf8K8Z51G15VYpucR2lGgentF8no-QT9T4QjOJluYb7TAdSEeOQ-nkoTAhYyqMOpTvnE_P2Nfz8PwW1VcL2s9V6VaXS7cqL1ps5WqZewNOzFvMjtHxckzavZUuvMfkCdosFUOi3hcQGGO9E44dTAHEgHmnkZdOUnfsRzF1fMvKQ1nEeTSQZg0b03_R5n3Q5K1dKNklv4bv78Anv91No9z8z73Wjg_6wedkp49NYdJNeUEemWqPPO3YKq_3yPasr8O_JH9Ru-DIEntclhJQ7Mt1WULScvfAFI7K9qwMLGwTiLKC5EJNIF3DvG7g1FjssdGA0TKkHRTM8lcAzpuh1wJ8bIdOzdqGtqiT0NTQ1hrAOq8O7o4r4WfZXNWvyFly8uN46vSkDk7O-LhxhFIc_QrlYUglZ0IXOrBJk_Qt90wh4jzi4yAwEVWWtQJvE-PFaFHIghoe7JOtqq7MGwIYaileUJaLwmdaS4VqUCgdxBrD0DjOR-TzINFs1fXuyNqch0YZKkHWKgHmPiPycRB3hsZlKyayMvVmndlj5j4KQ4Qj8roT_82bBr0ZEXFHMW4m2Mbdd0dQ3G0D7168bx-88gPZXnxJsu_p_NsBeYYxHOswie_IVnO1MYcYJzXqfWsR_wApXhEq |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+Borrelia+hermsii+factor+H+binding+protein+FhbA+is+not+required+for+infectivity+in+mice+or+for+resistance+to+human+complement+in+vitro&rft.jtitle=Infection+and+immunity&rft.au=Fine%2C+Lindy+M&rft.au=Miller%2C+Daniel+P&rft.au=Mallory%2C+Katherine+L&rft.au=Tegels%2C+Brittney+K&rft.date=2014-08-01&rft.eissn=1098-5522&rft.volume=82&rft.issue=8&rft.spage=3324&rft_id=info:doi/10.1128%2FIAI.01892-14&rft_id=info%3Apmid%2F24866803&rft.externalDocID=24866803 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0019-9567&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0019-9567&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0019-9567&client=summon |