Linked Life Data

19268337

Source:http://linkedlifedata.com/resource/pubmed/id/19268337

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-4-10
pubmed:abstractText
The ability of HIV to establish latent infection in CD4+ lymphocytes represents a major barrier to the eradication of HIV. It is not clear what mechanisms favor latent over productive infection, but prior studies have suggested a role for the viral transcription factor Tat or its RNA target, TAR. Using samples from five individuals who were started on ART within 6 months of infection and achieved a viral load <50 (suppressed), we isolated one- and two-exon tat RNA from HIV propagated ex vivo from baseline plasma and from co-cultures of CD4+ T cells obtained at baseline and suppressed time points. Compared to virus from the baseline plasma (mostly from productively-infected CD4+ T cells), virus from the baseline and suppressed co-cultures (mostly from latently-infected cells) had more Tat variants with impaired transactivation activity. These findings suggest that impaired activity in the Tat-TAR axis may contribute to the establishment of latent infection in CD4+ T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1096-0341
pubmed:author
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
387
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
98-108
pubmed:dateRevised
2011-3-14
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Latently-infected CD4+ T cells are enriched for HIV-1 Tat variants with impaired transactivation activity.
pubmed:affiliation
University of California, San Francisco (UCSF) and San Francisco VA Medical Center (SFVAMC), 4150 Clement Street, 111W3, San Francisco, CA 94121, USA. steven.yukl@ucsf.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural