Multivalent Group A Streptococcal Vaccine Elicits Bactericidal Antibodies against Variant M Subtypes
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Published in | Clinical and Diagnostic Laboratory Immunology Vol. 12; no. 7; pp. 833 - 836 |
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Format | Journal Article |
Language | English |
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American Society for Microbiology
01.07.2005
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ISSN | 1556-6811 1071-412X 1556-679X 1098-6588 |
DOI | 10.1128/CDLI.12.7.833-836.2005 |
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AbstractList | Group A streptococci cause a wide spectrum of clinical illness. One of several strategies for vaccine prevention of these infections is based on the type-specific M protein epitopes. A multivalent M protein-based vaccine containing type-specific determinants from 26 different M serotypes is now in clinical trials. Recent epidemiologic studies have shown that, within some serotypes, the amino-terminal M protein sequence may show natural variation, giving rise to subtypes. This raises the possibility that vaccine-induced antibodies against the parent type may not be as effective in promoting bactericidal killing of variant subtypes. In the present study we used rabbit antisera against the 26-valent M protein-based vaccine in bactericidal tests against M1, M3, and M5 streptococci, which were represented by multiple subtypes. We show that the vaccine antibodies effectively promoted in vitro bactericidal activity despite the fact that the M proteins contained naturally occurring variant sequences in the regions corresponding to the vaccine sequence. Our results show that the variant M proteins generally do not result in significant differences in opsonization promoted by rabbit antisera raised against the 26-valent vaccine, suggesting that a multivalent M protein vaccine may not permit variant subtypes of group A streptococci to escape in a highly immunized population. Group A streptococci cause a wide spectrum of clinical illness. One of several strategies for vaccine prevention of these infections is based on the type-specific M protein epitopes. A multivalent M protein-based vaccine containing type-specific determinants from 26 different M serotypes is now in clinical trials. Recent epidemiologic studies have shown that, within some serotypes, the amino-terminal M protein sequence may show natural variation, giving rise to subtypes. This raises the possibility that vaccine-induced antibodies against the parent type may not be as effective in promoting bactericidal killing of variant subtypes. In the present study we used rabbit antisera against the 26-valent M protein-based vaccine in bactericidal tests against M1, M3, and M5 streptococci, which were represented by multiple subtypes. We show that the vaccine antibodies effectively promoted in vitro bactericidal activity despite the fact that the M proteins contained naturally occurring variant sequences in the regions corresponding to the vaccine sequence. Our results show that the variant M proteins generally do not result in significant differences in opsonization promoted by rabbit antisera raised against the 26-valent vaccine, suggesting that a multivalent M protein vaccine may not permit variant subtypes of group A streptococci to escape in a highly immunized population.Group A streptococci cause a wide spectrum of clinical illness. One of several strategies for vaccine prevention of these infections is based on the type-specific M protein epitopes. A multivalent M protein-based vaccine containing type-specific determinants from 26 different M serotypes is now in clinical trials. Recent epidemiologic studies have shown that, within some serotypes, the amino-terminal M protein sequence may show natural variation, giving rise to subtypes. This raises the possibility that vaccine-induced antibodies against the parent type may not be as effective in promoting bactericidal killing of variant subtypes. In the present study we used rabbit antisera against the 26-valent M protein-based vaccine in bactericidal tests against M1, M3, and M5 streptococci, which were represented by multiple subtypes. We show that the vaccine antibodies effectively promoted in vitro bactericidal activity despite the fact that the M proteins contained naturally occurring variant sequences in the regions corresponding to the vaccine sequence. Our results show that the variant M proteins generally do not result in significant differences in opsonization promoted by rabbit antisera raised against the 26-valent vaccine, suggesting that a multivalent M protein vaccine may not permit variant subtypes of group A streptococci to escape in a highly immunized population. Classifications Services CVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue CVI About CVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy CVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1556-6811 Online ISSN: 1556-679X Copyright © 2014 by the American Society for Microbiology. For an alternate route to CVI .asm.org, visit: CVI |
Author | Bernard Beall Edna Y. Chiang James B. Dale Thomas Penfound Stanford T. Shulman Valerie Long |
AuthorAffiliation | Department of Veterans Affairs, and, 1 Department of Medicine, 2 Department of Molecular Sciences, The University of Tennessee Health Science Center, Memphis, Tennessee, 3 Department of Pediatrics, Feinberg School of Medicine, Northwestern University, and Division of Infectious Diseases, Children's Memorial Hospital, Chicago, Illinois, 4 Respiratory Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 5 |
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CitedBy_id | crossref_primary_10_1155_2010_956071 crossref_primary_10_1016_j_vaccine_2006_12_051 crossref_primary_10_1016_j_ymeth_2009_03_024 crossref_primary_10_1016_j_vaccine_2006_06_043 crossref_primary_10_5694_j_1326_5377_2007_tb01054_x crossref_primary_10_1016_j_vaccine_2014_05_017 crossref_primary_10_1128_IAI_01921_14 crossref_primary_10_1586_erv_09_133 crossref_primary_10_1038_s41598_020_80508_6 crossref_primary_10_1016_S1696_2818_14_70160_X crossref_primary_10_1086_444505 crossref_primary_10_1586_erv_09_33 crossref_primary_10_1007_s11908_012_0263_7 crossref_primary_10_1016_j_vaccine_2008_08_037 crossref_primary_10_1371_journal_pone_0198658 crossref_primary_10_1016_j_diagmicrobio_2006_01_025 crossref_primary_10_1016_j_vaccine_2006_07_052 crossref_primary_10_1007_s00467_010_1554_6 crossref_primary_10_1007_s10156_010_0084_2 crossref_primary_10_4161_hv_25506 crossref_primary_10_1038_icb_2009_29 crossref_primary_10_1128_mBio_00618_16 crossref_primary_10_1007_s10096_011_1385_9 |
Cites_doi | 10.1073/pnas.0404163101 10.3201/eid0502.990209 10.1007/BF00196680 10.1084/jem.110.2.271 10.1084/jem.106.4.525 10.1086/421949 10.1086/341409 10.1086/379050 10.4049/jimmunol.89.3.307 10.1128/IAI.70.4.2171-2177.2002 10.1086/315120 10.1016/0264-410X(96)00050-3 |
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Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 Corresponding author. Mailing address: 1030 Jefferson Avenue (11A), Memphis, TN 38104. Phone: (901) 577-7207. Fax: (901) 448-8231. E-mail: james.dale@med.va.gov. |
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References_xml | – volume: 101 start-page: 11833 year: 2004 ident: e_1_3_2_2_2 publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.0404163101 – ident: e_1_3_2_5_2 doi: 10.3201/eid0502.990209 – volume: 183 start-page: 299 year: 1994 ident: e_1_3_2_4_2 publication-title: Med. Microbiol. Immunol. doi: 10.1007/BF00196680 – volume: 110 start-page: 271 year: 1959 ident: e_1_3_2_9_2 publication-title: J. Exp. Med. doi: 10.1084/jem.110.2.271 – volume: 106 start-page: 525 year: 1957 ident: e_1_3_2_8_2 publication-title: J. Exp. Med. doi: 10.1084/jem.106.4.525 – volume: 39 start-page: 325 year: 2004 ident: e_1_3_2_13_2 publication-title: Clin. Infect. Dis. doi: 10.1086/421949 – ident: e_1_3_2_12_2 doi: 10.1086/341409 – ident: e_1_3_2_10_2 doi: 10.1086/379050 – volume: 89 start-page: 307 year: 1962 ident: e_1_3_2_7_2 publication-title: J. Immunol. doi: 10.4049/jimmunol.89.3.307 – ident: e_1_3_2_6_2 doi: 10.1128/IAI.70.4.2171-2177.2002 – volume: 180 start-page: 1921 year: 1999 ident: e_1_3_2_14_2 publication-title: J. Infect. Dis. doi: 10.1086/315120 – ident: e_1_3_2_11_2 – volume: 14 start-page: 944 year: 1996 ident: e_1_3_2_3_2 publication-title: Vaccine doi: 10.1016/0264-410X(96)00050-3 – reference: 10558949 - J Infect Dis. 1999 Dec;180(6):1921-8 – reference: 15306998 - Clin Infect Dis. 2004 Aug 1;39(3):325-32 – reference: 13475611 - J Exp Med. 1957 Oct 1;106(4):525-44 – reference: 8873386 - Vaccine. 1996 Jul;14(10):944-8 – reference: 14624386 - J Infect Dis. 2003 Nov 15;188(10):1587-92 – reference: 14461914 - J Immunol. 1962 Sep;89:307-13 – reference: 12115092 - Clin Infect Dis. 2002 Aug 1;35(3):268-76 – reference: 16163629 - Clin Infect Dis. 2005 Oct 15;41(8):1114-22 – reference: 10221877 - Emerg Infect Dis. 1999 Mar-Apr;5(2):247-53 – reference: 15282372 - Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11833-8 – reference: 7596313 - Med Microbiol Immunol. 1994 Dec;183(6):299-306 – reference: 13673139 - J Exp Med. 1959 Aug 1;110(2):271-92 – reference: 11895984 - Infect Immun. 2002 Apr;70(4):2171-7 |
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Reddit... Group A streptococci cause a wide spectrum of clinical illness. One of several strategies for vaccine prevention of these infections is based on the... |
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SubjectTerms | Amino Acid Sequence Animals Antibodies, Bacterial - immunology Antigens, Bacterial - immunology Epitopes - immunology Microbial Immunology Molecular Sequence Data Rabbits Serum Bactericidal Test Streptococcal Infections - immunology Streptococcal Infections - prevention & control Streptococcal Vaccines - administration & dosage Streptococcal Vaccines - immunology Streptococcus Streptococcus - immunology |
Title | Multivalent Group A Streptococcal Vaccine Elicits Bactericidal Antibodies against Variant M Subtypes |
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