Source:http://linkedlifedata.com/resource/pubmed/id/15916792
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2005-6-13
|
pubmed:abstractText |
The mechanisms underlying the pathogenicity of CCR5-restricted (R5) human immunodeficiency virus type-1 (HIV-1) strains are incompletely understood. Acquisition or enhancement of macrophage (M)-tropism by R5 viruses contributes to R5 HIV-1 pathogenesis. In this study, we show that M-tropic R5 viruses isolated from individuals with acquired immunodeficiency syndrome (late R5 viruses) require lower levels of CD4/CCR5 expression for entry, have decreased sensitivity to inhibition by the entry inhibitors TAK-779 and T-20, and have increased sensitivity to neutralization by the Env MAb IgG1b12 compared with non-M-tropic R5 viruses isolated from asymptomatic, immunocompetent individuals (early R5 viruses). Augmenting CCR5 expression levels on monocyte-derived macrophages via retroviral transduction led to a complete or marginal restoration of M-tropism by early R5 viruses, depending on the viral strain. Thus, reduced CD4/CCR5 dependence is a phenotype of R5 HIV-1 associated with M-tropism and late stage infection, which may affect the efficacy of HIV-1 entry inhibitors.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Jul
|
pubmed:issn |
0042-6822
|
pubmed:author |
pubmed-author:ChurchillMelissaM,
pubmed-author:CroweSuzanne MSM,
pubmed-author:CunninghamAnthony LAL,
pubmed-author:ElleryPhilipP,
pubmed-author:GorryPaul RPR,
pubmed-author:GrayLachlanL,
pubmed-author:LewinSharon RSR,
pubmed-author:NasrNajlaN,
pubmed-author:SterjovskiJasminkaJ,
pubmed-author:WesselinghSteven LSL
|
pubmed:issnType |
Print
|
pubmed:day |
5
|
pubmed:volume |
337
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
384-98
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:15916792-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:15916792-Antigens, CD,
pubmed-meshheading:15916792-Antigens, CD4,
pubmed-meshheading:15916792-Cell Differentiation,
pubmed-meshheading:15916792-Cell Line,
pubmed-meshheading:15916792-HIV-1,
pubmed-meshheading:15916792-Humans,
pubmed-meshheading:15916792-Kidney,
pubmed-meshheading:15916792-Macrophages,
pubmed-meshheading:15916792-Monocytes,
pubmed-meshheading:15916792-Receptors, CCR5,
pubmed-meshheading:15916792-Receptors, HIV
|
pubmed:year |
2005
|
pubmed:articleTitle |
Uncoupling coreceptor usage of human immunodeficiency virus type 1 (HIV-1) from macrophage tropism reveals biological properties of CCR5-restricted HIV-1 isolates from patients with acquired immunodeficiency syndrome.
|
pubmed:affiliation |
Macfarlane Burnet Institute for Medical Research and Public Health, GPO Box 2284, Melbourne, 3001 Victoria, Australia; Department of Microbiology and Immunology, University of Melbourne, Victoria, Australia.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|