Source:http://linkedlifedata.com/resource/pubmed/id/21310820
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2011-5-2
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pubmed:abstractText |
The dynamics of immune cell populations during acute HIV-1 infection are not fully deciphered, especially for non-T cells. In this study, we tested whether specific cellular subsets of the innate arm of the immune response are affected early after HIV-1 infection. Using a cohort of HIV-1-infected individuals, we have monitored the relative frequency of blood T lymphocytes, monocytes, and DCs at various infection stages and measured their respective intracellular HIV-1 DNA loads. The HIV-1 DNA load in naive CD4(+) T lymphocytes, which are lost very early during acute infection, was ten- to 100-fold lower than in CD57(-) and CD57(+) memory CD4(+) T lymphocytes. We observed that despite rapid, persistent loss after HIV-1 infection, pDCs represented a non-negligible HIV-1 DNA reservoir. CD16(+) proinflammatory cDCs and monocytes accumulated gradually, and HIV-infected CD16(+) monocytes contained higher HIV-1 DNA loads than their CD16(-) counterpart during acute infection. During chronic infection, CD16(+) cDCs exhibited higher HIV-1 DNA loads than the CD16(-) population. Overall, our results demonstrate that non-T cell compartments are a major HIV-1 DNA reservoir, and CD16(+) monocytes and CD16(+) cDCs potentially play an important role in HIV-1 dissemination.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1938-3673
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pubmed:author |
pubmed-author:BakkerMargreetM,
pubmed-author:BerkhoutBenB,
pubmed-author:CentlivreMireilleM,
pubmed-author:GrijsenMarlous LML,
pubmed-author:JurriaansSuzanneS,
pubmed-author:LegrandNicolasN,
pubmed-author:PaxtonWilliam AWA,
pubmed-author:PollakisGeorgiosG,
pubmed-author:PrinsJan MJM,
pubmed-author:SteingroverRadjinR,
pubmed-author:van der SluisReneeR
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pubmed:issnType |
Electronic
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pubmed:volume |
89
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
785-95
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pubmed:meshHeading |
pubmed-meshheading:21310820-Acute Disease,
pubmed-meshheading:21310820-Adolescent,
pubmed-meshheading:21310820-Adult,
pubmed-meshheading:21310820-Chronic Disease,
pubmed-meshheading:21310820-DNA, Viral,
pubmed-meshheading:21310820-Dendritic Cells,
pubmed-meshheading:21310820-Disease Progression,
pubmed-meshheading:21310820-Female,
pubmed-meshheading:21310820-Flow Cytometry,
pubmed-meshheading:21310820-HIV Infections,
pubmed-meshheading:21310820-HIV-1,
pubmed-meshheading:21310820-Humans,
pubmed-meshheading:21310820-Lymphocyte Count,
pubmed-meshheading:21310820-Male,
pubmed-meshheading:21310820-Middle Aged,
pubmed-meshheading:21310820-Monocytes,
pubmed-meshheading:21310820-Myeloid Cells,
pubmed-meshheading:21310820-RNA, Messenger,
pubmed-meshheading:21310820-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21310820-T-Lymphocyte Subsets,
pubmed-meshheading:21310820-Young Adult
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pubmed:year |
2011
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pubmed:articleTitle |
Altered dynamics and differential infection profiles of lymphoid and myeloid cell subsets during acute and chronic HIV-1 infection.
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pubmed:affiliation |
Laboratories of Experimental Virology, Department of Medical Microbiology, Center for Infection andImmunity Amsterdam, Tropical Medicine and AIDS, Academic Medical Center of the University of Amsterdam, Amsterdam, The Netherlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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