ArticleClinical and experimental immunology2002
Regulation of primary HIV-1 isolate replication in dendritic cells.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 26 citations in OpenAlex.
- HIV-1 Tat and Viral Latency: What We Can Learn from Naturally Occurring Sequence Variations.Frontiers in microbiology · 2017Review
- Review
- Review
- Cellular reservoirs of HIV-1 and their role in viral persistence.Current HIV research · 2008Review
- Dendritic cells in viral pathogenesis: protective or defective?International journal of experimental pathology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The potential role of dendritic cells (DC) in the immunopathology of human immunodeficiency virus 1 (HIV-1) disease remains controversial. This study examines replication of a panel of HIV-1 strains (both laboratory adapted and primary) within DC, in the context of the well-established monocyte-DC and monocyte-macrophage transition. Viral replication was assessed by p24 ELISA assay. All strains of HIV-1 tested replicated in DC. Only CCR5-tropic virus replicated in macrophages. Lipopolysaccharide (LPS) induced DC maturation (as reflected in altered cell phenotype) and at the same time diminished the ability of DC to support HIV-1 replication. In contrast the presence of activated T cells, which had been fixed to prevent them acting as a site for viral replication, enhanced the ability of the DC to support viral replication, as has been reported previously for macrophages. Thus cells that are DC by phenotype, but are not activated, act as the optimum reservoir for HIV-1 replication. If this form of DC is present in peripheral tissues, this will be permissive for amplification of the in vivo viral load at sites where there are few responder cells available, and hence contribute to the persistent immunopathology.
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What OpenQuestion holds
Registered trials
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.