Linked Life Data

17083039

Source:http://linkedlifedata.com/resource/pubmed/id/17083039

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-11-3
pubmed:abstractText
Pertussis toxin (PTX) and its binding unit (PTX-B) have been shown to inhibit human immunodeficiency virus (HIV)-1 infection of primary cells. However, the anti-HIV mechanisms have yet to be defined. We demonstrate that PTX inhibits HIV-1 infection of human cervical tissue independently of viral tropism. PTX-B showed a similar pattern of HIV-1 inhibition. Further investigation in macrophages demonstrated that PTX/PTX-B inhibited HIV-1 expression but that other G protein inhibitors and activators had no effect on HIV-1 replication. Unlike the anti-HIV bacterial lipopolysaccharide, the anti-HIV effects of PTX/PTX-B were not due to beta -chemokine production or coreceptor down-modulation, but they were dependent on interaction with cell-surface receptors. Antibody blocking studies suggested that cell-surface CD14 is very likely to be the principal receptor involved in the anti-HIV effects of PTX/PTX-B. This was further strengthened by the results of surface plasmon resonance analyses. Further definition of the mechanisms of such inhibition may lead to the development of novel HIV-1 prevention strategies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
194
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1547-56
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Pertussis toxin and its binding unit inhibit HIV-1 infection of human cervical tissue and macrophages involving a CD14 pathway.
pubmed:affiliation
Center for Infection, Department of Cellular and Molecular Medicine, St. George's University of London, London SW17 0RE, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural