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rdf:type |
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lifeskim:mentions |
umls-concept:C0019704,
umls-concept:C0021311,
umls-concept:C0022702,
umls-concept:C0030705,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0243127,
umls-concept:C0443331,
umls-concept:C0887947,
umls-concept:C1332714,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1706438,
umls-concept:C2698600
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pubmed:issue |
25
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pubmed:dateCreated |
2000-12-18
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pubmed:abstractText |
To evaluate the effects of HIV infection on T cell turnover, we examined levels of DNA synthesis in lymph node and peripheral blood mononuclear cell subsets by using ex vivo labeling with BrdUrd. Compared with healthy controls (n = 67), HIV-infected patients (n = 57) had significant increases in the number and fraction of dividing CD4(+) and CD8(+) T cells. Higher percentages of dividing CD4(+) and CD8(+) T cells were noted in patients with the higher viral burdens. No direct correlation was noted between rates of T cell turnover and CD4(+) T cell counts. Marked reductions in CD4(+) and CD8(+) T cell proliferation were seen in 11/11 patients 1-12 weeks after initiation of highly active antiretroviral therapy (HAART). These reductions persisted for the length of the study (16-72 weeks). Decreases in naive T cell proliferation correlated with increases in the levels of T cell receptor rearrangement excision circles. Division of CD4(+) and CD8(+) T cells increased dramatically in association with rapid increases in HIV-1 viral loads in 9/9 patients 5 weeks after termination of HAART and declined to pre-HAART-termination levels 8 weeks after reinitiation of therapy. These data are consistent with the hypothesis that HIV-1 infection induces a viral burden-related, global activation of the immune system, leading to increases in lymphocyte proliferation.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10477556,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10523562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10607709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10611346,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10712441,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-10805798,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-2582258,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-7529365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-7746312,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-7746313,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-7746314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-7816094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-8145034,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9021206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9448301,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9461195,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9469816,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9500797,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9547340,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9600975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9662370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9872319,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11095734-9883844
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0027-8424
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pubmed:author |
pubmed-author:AdelsbergerJ WJW,
pubmed-author:AlvordW GWG,
pubmed-author:BaselerM WMW,
pubmed-author:BoscheM CMC,
pubmed-author:DavidS LSL,
pubmed-author:DewarR LRL,
pubmed-author:DimitrovD SDS,
pubmed-author:KovacsJ AJA,
pubmed-author:LambertL ALA,
pubmed-author:LaneH CHC,
pubmed-author:LempickiR ARA,
pubmed-author:MetcalfJ AJA,
pubmed-author:NatarajanVV,
pubmed-author:PolisM AMA,
pubmed-author:StevensR ARA
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pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
97
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13778-83
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11095734-Antigens, CD45,
pubmed-meshheading:11095734-Antiretroviral Therapy, Highly Active,
pubmed-meshheading:11095734-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11095734-CD8-Positive T-Lymphocytes,
pubmed-meshheading:11095734-Cell Division,
pubmed-meshheading:11095734-Flow Cytometry,
pubmed-meshheading:11095734-HIV Infections,
pubmed-meshheading:11095734-HIV-1,
pubmed-meshheading:11095734-Humans,
pubmed-meshheading:11095734-Receptors, Antigen, T-Cell
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pubmed:year |
2000
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pubmed:articleTitle |
Impact of HIV-1 infection and highly active antiretroviral therapy on the kinetics of CD4+ and CD8+ T cell turnover in HIV-infected patients.
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pubmed:affiliation |
Science Applications International Corporation-Frederick, Clinical Services Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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