Evidence map›Paper›PMID 11444382›Full record

ArticleImmunologic research2001

T cell signaling mechanisms that regulate HIV-1 infection.

D Unutmaz

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
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

1 author.

D UnutmazVanderbilt University Medical School, Department of Microbiology and Immunology, Nashville, TN 31232, USA. derya.unutmaz@mcmail.vanderbilt.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of human immunodeficiency virus type-1 (HIV-1) to establish a persistent infection is critically dependent on the cellular signals that regulate HIV-1 replication within target cells. The balance between numerous host factors that either enhance or suppress viral infection determines the clinical outcome. Perturbation of the steady-state level of viral replication can significantly influence the course and the speed at which the infection develops into clinical disease. Activation signals delivered to T cells by cytokines and antigen-presenting cells (APC), are key modulators of viral replication. Our laboratory seeks to decipher how HIV-1 exploits T cell signaling mechanisms and host factors that regulate viral replication. Elucidation of the molecular mechanisms by which cellular signals regulate the HIV-1 life cycle within target cells will significantly advance our understanding of host-virus interactions.

Indexed as

Cell Adhesion MoleculesLectins, C-TypeAntigen-Presenting CellsCD4-Positive T-LymphocytesCytokinesDC-Specific ICAM-3 Grabbing NonintegrinDendritic CellsGene Products, nefHIV-1HIV InfectionsHumansImmunologic MemoryLectinsLymphocyte ActivationLymphoid Tissuenef Gene Products, Human Immunodeficiency VirusCell Adhesion MoleculesCytokinesDC-Specific ICAM-3 Grabbing NonintegrinGene Products, nefLectinsLectins, C-Typenef Gene Products, Human Immunodeficiency VirusReceptors, Cell Surface

Identifiers

PMID11444382

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.