Evidence map›Paper›PMID 10639161›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Functional deletion of the CCR5 receptor by intracellular immunization produces cells that are refractory to CCR5-dependent HIV-1 infection and cell fusion.

P Steinberger, J Andris-Widhopf, B Bühler, B E Torbett, C F Barbas

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 114 citations in OpenAlex.

  1. Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020
    Review
  2. mRNA as novel technology for passive immunotherapy.Cellular and molecular life sciences : CMLS · 2019
    Review
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  16. Zinc-finger nuclease editing of human cxcr4 promotes HIV-1 CD4(+) T cell resistance and enrichment.Molecular therapy : the journal of the American Society of Gene Therapy · 2012
    Article
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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

5 authors at 1 institution in 1 country.

P SteinbergerSkaggs Institute for Chemical Biology and Department of Molecular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
J Andris-Widhopf
B Bühler
B E Torbett
C F Barbas
Scripps Research Institute · US

Funding

CHEMOKINE RECEPTOR ANTAGONISTS FOR HIV1 THERAPYR01AI041944 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI BARBAS, CARLOS F · 1997 to 2000
$375k
NIAID NIH HHS 5F32 AI04397-03NIAID NIH HHS AI41944PHS HHS DL49886
6 · The paper itself

Abstract

Studies of naturally occurring polymorphisms of the CCR5 gene have shown that deletion of the functional receptor or reduced expression of the gene can have beneficial effects in preventing HIV-1 infection or delaying disease. Because these polymorphisms are found in otherwise healthy people, strategies that aim to prevent or limit expression of CCR5 should be beneficial in the treatment of HIV-1 disease. To test this approach we have developed a CCR5-specific single-chain antibody that was expressed intracellularly and retained in the endoplasmic reticulum. This CCR5-intrabody efficiently blocked surface expression of human and rhesus CCR5 and thus prevented cellular interactions with CCR5-dependent HIV-1 and simian immunodeficiency virus envelope glycoprotein. Intrabody-expressing cells were shown to be highly refractory to challenge with R5 HIV-1 viruses or infected cells. These results suggest that gene therapy approaches that deliver this intracellular antibody could be of benefit to infected individuals. Because the antibody reacts with a conserved primate epitope on CCR5 this strategy can be tested in nonhuman lentivirus models of HIV-1 disease.

Indexed as

ImmunizationAnimalsAntibodies, MonoclonalCell FusionCell LineCOS CellsGene Expression RegulationGene Products, envHIV-1HIV InfectionsHumansMacaca mulattaPlasmidsReceptors, CCR5Receptors, Cell SurfaceTransfectionAntibodies, MonoclonalGene Products, envReceptors, CCR5Receptors, Cell Surface

Identifiers

PMID10639161
PMCPMC15412
OpenAlexW2029788603

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.