Linked Life Data

10486921

Source:http://linkedlifedata.com/resource/pubmed/id/10486921

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1999-10-18
pubmed:abstractText
Vibrio cholerae O1 strains are classified into one of two biotypes, classical and E1 Tor, the latter being primarily responsible for cholera cases worldwide since 1961. Recent studies in our laboratory have focused upon the pathogenic and vaccine significance of the toxin-coregulated pili (TCP) produced by strains of E1 Tor biotype. Mutants in which the tcpA gene (encoding the pilin subunit protein) has been inactivated are dramatically attenuated in the infant mouse cholera model, showing markedly reduced colonisation potential in mixed-infection competition experiments. Significantly, in the vaccine context, antibodies to TCP are sufficient to prevent experimental infection, although our data suggest that this protective effect might be limited to strains of homologous biotype. Since we have shown that tcpA sequences are conserved within a biotype but differ between biotypes, this latter observation suggests that the biotype-restricted pilin epitopes might have greater vaccine significance. Similar studies indicate that TCP also play a critical role in colonisation by strains of the recently-recognised O139 serogroup, which is thought to have evolved from an O1 E1 Tor strain. In contrast to the effect of introducing mutations in the tcpA gene, strains carrying inactivated mshA genes (encoding the subunit of the mannose-sensitive haemagglutinin pilus) show unaltered in vivo behaviour. Consistent with this finding is our inability to demonstrate any protective effect associated with antibodies to MSHA. Ongoing approaches to vaccine development are variously aimed at improving the immunogenicity of the current inactivated whole-cell vaccine, or assessing the field efficacy of a promising live attenuated strain. The possible implications of our findings are discussed in relation to both of these options.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0168-1656
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
109-17
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10486921-Animals, pubmed-meshheading:10486921-Antibodies, Bacterial, pubmed-meshheading:10486921-Bacterial Outer Membrane Proteins, pubmed-meshheading:10486921-Bacterial Proteins, pubmed-meshheading:10486921-Bacterial Typing Techniques, pubmed-meshheading:10486921-Biotechnology, pubmed-meshheading:10486921-Cholera, pubmed-meshheading:10486921-Cholera Toxin, pubmed-meshheading:10486921-Cholera Vaccines, pubmed-meshheading:10486921-Fimbriae, Bacterial, pubmed-meshheading:10486921-Fimbriae Proteins, pubmed-meshheading:10486921-Genes, Bacterial, pubmed-meshheading:10486921-Hemagglutinins, pubmed-meshheading:10486921-Humans, pubmed-meshheading:10486921-Mannose-Binding Lectin, pubmed-meshheading:10486921-Mice, pubmed-meshheading:10486921-Mutation, pubmed-meshheading:10486921-Vibrio cholerae
pubmed:year
1999
pubmed:articleTitle
Pathogenic and vaccine significance of toxin-coregulated pili of Vibrio cholerae E1 Tor.
pubmed:affiliation
Department of Microbiology and Immunology, University of Adelaide, Australia. sattridg@microb.adelaide.edu.au
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't