Evidence map›Paper›PMID 12011460›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Persistent HIV-1 infection of natural killer cells in patients receiving highly active antiretroviral therapy.

Antonio Valentin, Margherita Rosati, Daniel J Patenaude, Angelos Hatzakis, Leondios G Kostrikis, Marios Lazanas, Kathleen M Wyvill, Robert Yarchoan, George N Pavlakis

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 162 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Antonio ValentinHuman Retrovirus Section, Basic Research Laboratory, National Cancer Institute, Frederick, MD 21702, USA.
Margherita Rosati
Daniel J Patenaude
Angelos Hatzakis
Leondios G Kostrikis
Marios Lazanas
Kathleen M Wyvill
Robert Yarchoan
George N Pavlakis
Hellenic Red Cross · GRNational and Kapodistrian University of Athens · GRNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have identified a subset of CD56(+)CD3(-) human natural killer (NK) cells that express CD4 and the HIV coreceptors CCR5 and CXCR4. These cells can be productively infected in vitro by both CCR5- and CXCR4-using molecular clones of HIV-1 in a CD4-dependent manner. Analysis of HIV-infected persons showed that viral DNA is present in purified NK cells, and virus could be rescued from these cells after in vitro cultivation. Longitudinal analysis of the HIV-1 DNA levels in NK cells from patients after 1-2 years of highly active antiretroviral therapy indicated that NK cells remain persistently infected and account for a substantial amount of the viral DNA in peripheral blood mononuclear cells. These results demonstrate that a subset of non-T cells with NK markers are persistently infected and suggest that HIV infection of NK cells is important for virus persistence. The properties of the virus reservoir in these cells should be considered in attempts to further optimize antiretroviral therapies.

Indexed as

CD56 AntigenAnti-HIV AgentsAntiretroviral Therapy, Highly ActiveCD4 AntigensCD4-Positive T-LymphocytesHIV-1HIV InfectionsHumansKiller Cells, NaturalLymphocyte SubsetsReceptors, CCR5Receptors, CXCR4Anti-HIV AgentsCD4 AntigensCD56 AntigenReceptors, CCR5Receptors, CXCR4

Identifiers

PMID12011460
PMCPMC124520
OpenAlexW2132008472

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.