Molecular determinants of disease in coxsackievirus B1 murine infection

Autores
Cifuente, Javier O.; Ferrer, María Florencia; Jaquenod De Giusti, Carolina; Song, Wen Chao; Romanowski, Víctor; Hafenstein, Susan; Gómez, Ricardo Martín
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
To understand better how different genomic regions may confer pathogenicity for the coxsackievirus B (CVB), two intratypic CVB1 variants and a number of recombinant viruses were studied. Sequencing analysis showed 23 nucleotide changes between the parental non-pathogenic CVB1N and the pathogenic CVB1Nm. Mutations present in CVB1Nm were more conserved than those in CVB1N when compared to other CVB sequences. Inoculation in C3H/HeJ mice showed that the P1 region is critical for pathogenicity in murine pancreas and heart. The molecular determinants of disease for these organs partially overlap. Several P1 region amino acid differences appear to be located in the decay accelerating factor (DAF) footprint CVBs. CVB1N and CVB1Nm interacted with human CAR, but only CVB1N seemed to interact with human DAF, as determined using soluble receptors in a plaque reduction assay. However, the murine homologue Daf-1 did not interact with any virus assessed by haemagglutination. The results of this study suggest that an unknown receptor interaction with the virus play an important role in the pathogenicity of CVB1Nm. Further in vivo studies may clarify this issue.
Instituto de Biotecnología y Biología Molecular
Materia
Ciencias Exactas
Química
pancreatitis
myocarditis
DAF
CAR
mice
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/127313
Acceder
id SEDICI_7f76ca7da6bf4ffed804f6d5f030bf3f
oai_identifier_str oai:sedici.unlp.edu.ar:10915/127313
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Molecular determinants of disease in coxsackievirus B1 murine infectionCifuente, Javier O.Ferrer, María FlorenciaJaquenod De Giusti, CarolinaSong, Wen ChaoRomanowski, VíctorHafenstein, SusanGómez, Ricardo MartínCiencias ExactasQuímicapancreatitismyocarditisDAFCARmiceTo understand better how different genomic regions may confer pathogenicity for the coxsackievirus B (CVB), two intratypic CVB1 variants and a number of recombinant viruses were studied. Sequencing analysis showed 23 nucleotide changes between the parental non-pathogenic CVB1N and the pathogenic CVB1Nm. Mutations present in CVB1Nm were more conserved than those in CVB1N when compared to other CVB sequences. Inoculation in C3H/HeJ mice showed that the P1 region is critical for pathogenicity in murine pancreas and heart. The molecular determinants of disease for these organs partially overlap. Several P1 region amino acid differences appear to be located in the decay accelerating factor (DAF) footprint CVBs. CVB1N and CVB1Nm interacted with human CAR, but only CVB1N seemed to interact with human DAF, as determined using soluble receptors in a plaque reduction assay. However, the murine homologue Daf-1 did not interact with any virus assessed by haemagglutination. The results of this study suggest that an unknown receptor interaction with the virus play an important role in the pathogenicity of CVB1Nm. Further <i>in vivo</i> studies may clarify this issue.Instituto de Biotecnología y Biología Molecular2011-07-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf1571-1581http://sedici.unlp.edu.ar/handle/10915/127313enginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1002/jmv.22133?__cf_chl_jschl_tk__=pmd_TYe1oxqEE5xuOqdGUt3a4GPE9MkF4Wt2_ZxBPatX4fo-1635269542-0-gqNtZGzNAiWjcnBszQtRinfo:eu-repo/semantics/altIdentifier/issn/1096-9071info:eu-repo/semantics/altIdentifier/issn/0146-6615info:eu-repo/semantics/altIdentifier/pmid/21739448info:eu-repo/semantics/altIdentifier/doi/10.1002/jmv.22133info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-11-12T10:54:58Zoai:sedici.unlp.edu.ar:10915/127313Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-11-12 10:54:58.478SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Molecular determinants of disease in coxsackievirus B1 murine infection
title Molecular determinants of disease in coxsackievirus B1 murine infection
spellingShingle Molecular determinants of disease in coxsackievirus B1 murine infection
Cifuente, Javier O.
Ciencias Exactas
Química
pancreatitis
myocarditis
DAF
CAR
mice
title_short Molecular determinants of disease in coxsackievirus B1 murine infection
title_full Molecular determinants of disease in coxsackievirus B1 murine infection
title_fullStr Molecular determinants of disease in coxsackievirus B1 murine infection
title_full_unstemmed Molecular determinants of disease in coxsackievirus B1 murine infection
title_sort Molecular determinants of disease in coxsackievirus B1 murine infection
dc.creator.none.fl_str_mv Cifuente, Javier O.
Ferrer, María Florencia
Jaquenod De Giusti, Carolina
Song, Wen Chao
Romanowski, Víctor
Hafenstein, Susan
Gómez, Ricardo Martín
author Cifuente, Javier O.
author_facet Cifuente, Javier O.
Ferrer, María Florencia
Jaquenod De Giusti, Carolina
Song, Wen Chao
Romanowski, Víctor
Hafenstein, Susan
Gómez, Ricardo Martín
author_role author
author2 Ferrer, María Florencia
Jaquenod De Giusti, Carolina
Song, Wen Chao
Romanowski, Víctor
Hafenstein, Susan
Gómez, Ricardo Martín
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Exactas
Química
pancreatitis
myocarditis
DAF
CAR
mice
topic Ciencias Exactas
Química
pancreatitis
myocarditis
DAF
CAR
mice
dc.description.none.fl_txt_mv To understand better how different genomic regions may confer pathogenicity for the coxsackievirus B (CVB), two intratypic CVB1 variants and a number of recombinant viruses were studied. Sequencing analysis showed 23 nucleotide changes between the parental non-pathogenic CVB1N and the pathogenic CVB1Nm. Mutations present in CVB1Nm were more conserved than those in CVB1N when compared to other CVB sequences. Inoculation in C3H/HeJ mice showed that the P1 region is critical for pathogenicity in murine pancreas and heart. The molecular determinants of disease for these organs partially overlap. Several P1 region amino acid differences appear to be located in the decay accelerating factor (DAF) footprint CVBs. CVB1N and CVB1Nm interacted with human CAR, but only CVB1N seemed to interact with human DAF, as determined using soluble receptors in a plaque reduction assay. However, the murine homologue Daf-1 did not interact with any virus assessed by haemagglutination. The results of this study suggest that an unknown receptor interaction with the virus play an important role in the pathogenicity of CVB1Nm. Further <i>in vivo</i> studies may clarify this issue.
Instituto de Biotecnología y Biología Molecular
description To understand better how different genomic regions may confer pathogenicity for the coxsackievirus B (CVB), two intratypic CVB1 variants and a number of recombinant viruses were studied. Sequencing analysis showed 23 nucleotide changes between the parental non-pathogenic CVB1N and the pathogenic CVB1Nm. Mutations present in CVB1Nm were more conserved than those in CVB1N when compared to other CVB sequences. Inoculation in C3H/HeJ mice showed that the P1 region is critical for pathogenicity in murine pancreas and heart. The molecular determinants of disease for these organs partially overlap. Several P1 region amino acid differences appear to be located in the decay accelerating factor (DAF) footprint CVBs. CVB1N and CVB1Nm interacted with human CAR, but only CVB1N seemed to interact with human DAF, as determined using soluble receptors in a plaque reduction assay. However, the murine homologue Daf-1 did not interact with any virus assessed by haemagglutination. The results of this study suggest that an unknown receptor interaction with the virus play an important role in the pathogenicity of CVB1Nm. Further <i>in vivo</i> studies may clarify this issue.
publishDate 2011
dc.date.none.fl_str_mv 2011-07-07
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/127313
url http://sedici.unlp.edu.ar/handle/10915/127313
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1002/jmv.22133?__cf_chl_jschl_tk__=pmd_TYe1oxqEE5xuOqdGUt3a4GPE9MkF4Wt2_ZxBPatX4fo-1635269542-0-gqNtZGzNAiWjcnBszQtR
info:eu-repo/semantics/altIdentifier/issn/1096-9071
info:eu-repo/semantics/altIdentifier/issn/0146-6615
info:eu-repo/semantics/altIdentifier/pmid/21739448
info:eu-repo/semantics/altIdentifier/doi/10.1002/jmv.22133
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
dc.format.none.fl_str_mv application/pdf
1571-1581
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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