Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/30855 http://dx.doi.org/10.1371/journal.pone.0003026 |
Resumo: | Outbreaks of disease attributable to human error or natural causes can provide unique opportunities to gain new information about host-pathogen interactions and new leads for pathogenesis research. Poststreptococcal glomerulonephritis (PSGN), a sequela of infection with pathogenic streptococci, is a common cause of preventable kidney disease worldwide. Although PSGN usually occurs after infection with group A streptococci, organisms of Lancefield group C and G also can be responsible. Despite decades of study, the molecular pathogenesis of PSGN is poorly understood. As a first step toward gaining new information about PSGN pathogenesis, we sequenced the genome of Streptococcus equi subsp. zooepidemicus strain MGCS10565, a group C organism that caused a very large and unusually severe epidemic of nephritis in Brazil. the genome is a circular chromosome of 2,024,171 bp. the genome shares extensive gene content, including many virulence factors, with genetically related group A streptococci, but unexpectedly lacks prophages. the genome contains many apparently foreign genes interspersed around the chromosome, consistent with the presence of a full array of genes required for natural competence. An inordinately large family of genes encodes secreted extracellular collagen-like proteins with multiple integrin-binding motifs. the absence of a gene related to speB rules out the long-held belief that streptococcal pyrogenic exotoxin B or antibodies reacting with it singularly cause PSGN. Many proteins previously implicated in GAS PSGN, such as streptokinase, are either highly divergent in strain MGCS10565 or are not more closely related between these species than to orthologs present in other streptococci that do not commonly cause PSGN. Our analysis provides a comparative genomics framework for renewed appraisal of molecular events underlying APSGN pathogenesis. |
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Beres, Stephen B.Sesso, Ricardo [UNIFESP]Pinto, Sergio Wyton L.Hoe, Nancy P.Porcella, Stephen F.Deleo, Frank R.Musser, James M.Methodist HospUniversidade Federal de São Paulo (UNIFESP)Hosp Sao Joao DeusNIH2016-01-24T13:51:38Z2016-01-24T13:51:38Z2008-08-21Plos One. San Francisco: Public Library Science, v. 3, n. 8, 16 p., 2008.1932-6203http://repositorio.unifesp.br/handle/11600/30855http://dx.doi.org/10.1371/journal.pone.0003026WOS000264426800005.pdf10.1371/journal.pone.0003026WOS:000264426800005Outbreaks of disease attributable to human error or natural causes can provide unique opportunities to gain new information about host-pathogen interactions and new leads for pathogenesis research. Poststreptococcal glomerulonephritis (PSGN), a sequela of infection with pathogenic streptococci, is a common cause of preventable kidney disease worldwide. Although PSGN usually occurs after infection with group A streptococci, organisms of Lancefield group C and G also can be responsible. Despite decades of study, the molecular pathogenesis of PSGN is poorly understood. As a first step toward gaining new information about PSGN pathogenesis, we sequenced the genome of Streptococcus equi subsp. zooepidemicus strain MGCS10565, a group C organism that caused a very large and unusually severe epidemic of nephritis in Brazil. the genome is a circular chromosome of 2,024,171 bp. the genome shares extensive gene content, including many virulence factors, with genetically related group A streptococci, but unexpectedly lacks prophages. the genome contains many apparently foreign genes interspersed around the chromosome, consistent with the presence of a full array of genes required for natural competence. An inordinately large family of genes encodes secreted extracellular collagen-like proteins with multiple integrin-binding motifs. the absence of a gene related to speB rules out the long-held belief that streptococcal pyrogenic exotoxin B or antibodies reacting with it singularly cause PSGN. Many proteins previously implicated in GAS PSGN, such as streptokinase, are either highly divergent in strain MGCS10565 or are not more closely related between these species than to orthologs present in other streptococci that do not commonly cause PSGN. Our analysis provides a comparative genomics framework for renewed appraisal of molecular events underlying APSGN pathogenesis.National Institute of Allergy and Infectious DiseasesMethodist Hosp, Ctr Mol & Translat Human Infect Dis Res, Res Inst, Houston, TX 77030 USAUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, São Paulo, BrazilHosp Sao Joao Deus, Div Nephrol, Divinopolis, BrazilNIH, Off Res Serv, Div Occupat Hlth & Safety, Hamilton, MT USANIH, NIAID, Rocky Mt Lab, Lab Human Bacterial Pathogenesis, Hamilton, MT USAUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, São Paulo, BrazilNational Institute of Allergy and Infectious Diseases: UO1-60595Web of Science16engPublic Library SciencePlos OneGenome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Diseaseinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000264426800005.pdfapplication/pdf681609${dspace.ui.url}/bitstream/11600/30855/1/WOS000264426800005.pdfb80aac3cf98c8cd442c81383ad078227MD51open accessTEXTWOS000264426800005.pdf.txtWOS000264426800005.pdf.txtExtracted texttext/plain93419${dspace.ui.url}/bitstream/11600/30855/2/WOS000264426800005.pdf.txt35a303d9ae48019e1fd78761f625e80eMD52open access11600/308552022-02-18 12:05:33.758open accessoai:repositorio.unifesp.br:11600/30855Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-02-18T15:05:33Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
title |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
spellingShingle |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease Beres, Stephen B. |
title_short |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
title_full |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
title_fullStr |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
title_full_unstemmed |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
title_sort |
Genome Sequence of a Lancefield Group C Streptococcus zooepidemicus Strain Causing Epidemic Nephritis: New Information about an Old Disease |
author |
Beres, Stephen B. |
author_facet |
Beres, Stephen B. Sesso, Ricardo [UNIFESP] Pinto, Sergio Wyton L. Hoe, Nancy P. Porcella, Stephen F. Deleo, Frank R. Musser, James M. |
author_role |
author |
author2 |
Sesso, Ricardo [UNIFESP] Pinto, Sergio Wyton L. Hoe, Nancy P. Porcella, Stephen F. Deleo, Frank R. Musser, James M. |
author2_role |
author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Methodist Hosp Universidade Federal de São Paulo (UNIFESP) Hosp Sao Joao Deus NIH |
dc.contributor.author.fl_str_mv |
Beres, Stephen B. Sesso, Ricardo [UNIFESP] Pinto, Sergio Wyton L. Hoe, Nancy P. Porcella, Stephen F. Deleo, Frank R. Musser, James M. |
description |
Outbreaks of disease attributable to human error or natural causes can provide unique opportunities to gain new information about host-pathogen interactions and new leads for pathogenesis research. Poststreptococcal glomerulonephritis (PSGN), a sequela of infection with pathogenic streptococci, is a common cause of preventable kidney disease worldwide. Although PSGN usually occurs after infection with group A streptococci, organisms of Lancefield group C and G also can be responsible. Despite decades of study, the molecular pathogenesis of PSGN is poorly understood. As a first step toward gaining new information about PSGN pathogenesis, we sequenced the genome of Streptococcus equi subsp. zooepidemicus strain MGCS10565, a group C organism that caused a very large and unusually severe epidemic of nephritis in Brazil. the genome is a circular chromosome of 2,024,171 bp. the genome shares extensive gene content, including many virulence factors, with genetically related group A streptococci, but unexpectedly lacks prophages. the genome contains many apparently foreign genes interspersed around the chromosome, consistent with the presence of a full array of genes required for natural competence. An inordinately large family of genes encodes secreted extracellular collagen-like proteins with multiple integrin-binding motifs. the absence of a gene related to speB rules out the long-held belief that streptococcal pyrogenic exotoxin B or antibodies reacting with it singularly cause PSGN. Many proteins previously implicated in GAS PSGN, such as streptokinase, are either highly divergent in strain MGCS10565 or are not more closely related between these species than to orthologs present in other streptococci that do not commonly cause PSGN. Our analysis provides a comparative genomics framework for renewed appraisal of molecular events underlying APSGN pathogenesis. |
publishDate |
2008 |
dc.date.issued.fl_str_mv |
2008-08-21 |
dc.date.accessioned.fl_str_mv |
2016-01-24T13:51:38Z |
dc.date.available.fl_str_mv |
2016-01-24T13:51:38Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Plos One. San Francisco: Public Library Science, v. 3, n. 8, 16 p., 2008. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/30855 http://dx.doi.org/10.1371/journal.pone.0003026 |
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1932-6203 |
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WOS000264426800005.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1371/journal.pone.0003026 |
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WOS:000264426800005 |
identifier_str_mv |
Plos One. San Francisco: Public Library Science, v. 3, n. 8, 16 p., 2008. 1932-6203 WOS000264426800005.pdf 10.1371/journal.pone.0003026 WOS:000264426800005 |
url |
http://repositorio.unifesp.br/handle/11600/30855 http://dx.doi.org/10.1371/journal.pone.0003026 |
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