Evidence map›Paper›PMID 10684270›Full record

ArticleJournal of virology2000

Inhibition of CD3/CD28-mediated activation of the MEK/ERK signaling pathway represses replication of X4 but not R5 human immunodeficiency virus type 1 in peripheral blood CD4(+) T lymphocytes.

W Popik, P M Pitha

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

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  14. R5 and X4 HIV envelopes induce distinct gene expression profiles in primary peripheral blood mononuclear cells.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  15. Article
  16. Article
  17. HIV envelope induces a cascade of cell signals in non-proliferating target cells that favor virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

W PopikOncology Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. wpopik@jhmi.edu
P M Pitha
Johns Hopkins University · US

Funding

HIV-1-INDUCED SIGNAL TRANSDUCTION;ROLE IN PATHOGENESISR01AI040838 · NIAID · JOHNS HOPKINS UNIVERSITY · PI PITHA-ROWE, PAULA M · 1997 to 1999
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NIAID NIH HHS AI40838NIAID NIH HHS AI42557NIMHD NIH HHS L60 MD003100
6 · The paper itself

Abstract

Binding of human immunodeficiency virus type 1 (HIV-1) to CD4 receptors induces multiple cellular signaling pathways, including the MEK/ERK cascade. While the interaction of X4 HIV-1 with CXCR4 does not seem to activate this pathway, viruses using CCR5 for entry efficiently activate MEK/ERK kinases (W. Popik, J. E. Hesselgesser, and P. M. Pitha, J. Virol. 72:6406-6413, 1998; W. Popik and P. M. Pitha, Virology 252:210-217, 1998). Since the importance of MEK/ERK in the initial steps of viral replication is poorly understood, we have examined the role of MEK/ERK signaling in the CD3- and CD28 (CD3/CD28)-mediated activation of HIV-1 replication in resting peripheral blood CD4(+) T lymphocytes infected with X4 or R5 HIV-1. We have found that the MEK/ERK inhibitor U0126 selectively inhibited CD3/CD28-stimulated replication of X4 HIV-1, while it did not affect the replication of R5 HIV-1. Inhibition of the CD3/CD28-stimulated MEK/ERK pathway did not affect the formation of the early proviral transcripts in cells infected with either X4 or R5 HIV-1, indicating that virus reverse transcription is not affected in the absence of MEK/ERK signaling. In contrast, the levels of nuclear provirus in cells infected with X4 HIV-1, detected by the formation of circular proviral DNA, was significantly lower in cells stimulated in the presence of MEK/ERK inhibitor than in the absence of the inhibitor. However, in cells infected with R5 HIV-1, the inhibition of the MEK/ERK pathway did not affect nuclear localization of the proviral DNA. These data suggest that the nuclear import of X4, but not R5, HIV-1 is dependent on a CD3/CD28-stimulated MEK/ERK pathway.

Indexed as

MAP Kinase Signaling SystemBiological TransportButadienesCD28 AntigensCD3 ComplexCD4 AntigensCD4-Positive T-LymphocytesCell NucleusCells, CulturedDNA, ViralDown-RegulationEnzyme ActivationEnzyme InhibitorsHIV-1HumansMitogen-Activated Protein Kinase KinasesButadienesCD28 AntigensCD3 ComplexCD4 AntigensDNA, ViralEnzyme InhibitorsMitogen-Activated Protein Kinase KinasesNitrilesReceptors, CXCR4U 0126

Identifiers

PMID10684270
PMCPMC111744
OpenAlexW2019079607

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.