Evidence map›Paper›PMID 9223324›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection.

C J Li, Y Ueda, B Shi, L Borodyansky, L Huang, Y Z Li, A B Pardee

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.0field-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

36 citing papers in PubMed, 110 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

7 authors at 3 institutions in 2 countries.

C J LiDivision of Cell Growth and Regulation, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA. cjli-mbcrr.harvard.edu
Y Ueda
B Shi
L Borodyansky
L Huang
Y Z Li
A B Pardee
Institute of Molecular and Cell Biology · RUDana-Farber Cancer Institute · USHarvard University · US

Funding

DNA TOPOISOMERASE I DRUGS AND HIV-1 CHEMOTHERAPYR01AI035576 · NIAID · DANA-FARBER CANCER INSTITUTE · PI PARDEE, ARTHUR B · 1994 to 1996
–
NIAID NIH HHS AI-35576
6 · The paper itself

Abstract

We report that human immunodeficiency virus type 1 (HIV-1) has evolved a self-perpetuating mechanism to actively generate cells permissive for productive and cytopathic infection. Only activated T cells can be productively infected, which leads to their rapid depletion (2 x 10(9)/day in an infected individual). Establishment of productive HIV-1 infection therefore requires continual activations from the large pool of quiescent T cells. Tat protein, which is secreted by infected cells, activated uninfected quiescent T cells in vitro and in vivo. These Tat-activated uninfected cells became highly permissive for productive HIV-1 infection. Activation of primary T cells by Tat protein involved integrin receptors and was associated with activation of mitogen-activated protein kinases, including ERK1 and JNK kinase. Accordingly, these primary T cells progressed from G0 to the late G1 phase of the cell cycle.

Indexed as

Calcium-Calmodulin-Dependent Protein KinasesCarrier ProteinsCells, CulturedEnzyme ActivationGene Products, tatHIV-1HIV InfectionsHumansIntegrinsJurkat CellsLymphocyte Activationtat Gene Products, Human Immunodeficiency VirusT-LymphocytesVirus ReplicationCalcium-Calmodulin-Dependent Protein KinasesCarrier ProteinsGene Products, tatIntegrinstat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID9223324
PMCPMC21566
OpenAlexW2130117483

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.