Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-3-13
pubmed:abstractText
The long terminal repeat (LTR) region of HIV-1 promotes and modulates proviral transcription. LTR genetic variability might influence viral replication and disease progression. Proviral LTR sequences from 32 HIV-1-infected individuals showing different rates of disease progression were examined. Non-progressors (NP, n = 11) were individuals with high and stable CD4 counts and persistently low or undetectable plasma HIV-RNA. Slow progressors (SP, n = 6) were subjects with minimal CD4 decays over time and low plasma HIV-RNA. Typical progressors (TP, n = 15) were individuals with chronic infection showing CD4 counts repeatedly below 500 cells/mul. The mutation frequency within distinct LTR functional regions involved in HIV-1 transcription were compared in these three groups of patients. No significant differences were observed in the mutation frequency in most LTR regulatory sites when comparing the three groups. However, changes in USF regulatory binding sites were more frequent in TP than in SP/NP, while changes in Sp1 binding sites were less common in the former. This is the first study examining the genetic variability of the HIV-1 LTR region in long-term non-progressors showing further divergent outcomes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0920-8569
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
111-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Genetic analysis of the long terminal repeat (LTR) promoter region in HIV-1-infected individuals with different rates of disease progression.
pubmed:affiliation
Department of Infectious Diseases, Hospital Carlos III, C/ Sinesio Delgado, 10, 28029, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't