Evidence map›Paper›PMID 23202514›Full record

ReviewViruses2012

HIV-1 induced bystander apoptosis.

Himanshu Garg, Jonathon Mohl, Anjali Joshi

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The STAT Signaling Pathway in HIV-1 Infection: Roles and Dysregulation.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Human Immunodeficiency Virus Related Non-Hodgkin's Lymphoma.Blood and lymphatic cancer : targets and therapy · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Himanshu GargCenter of Excellence for Infectious Disease, Department of Biomedical Science, Texas Tech University Health Sciences Center, 5001 El Paso Dr, MSB-1 Annex, El Paso, TX 79905, USA. himanshu.garg@ttuhsc.edu
Jonathon Mohl
Anjali Joshi
Texas Tech University Health Sciences Center · USTexas Tech University · US

Funding

TARGETING THE VIRUS ASSEMBLY AND ENTRY PATHWAYS FOR ANTI-HIV GENE THERAPYR03AI095040 · NIAID · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI JOSHI, ANJALI · 2012 to 2013
$151k
NIAID NIH HHS 1R03AI095040-01A1NIAID NIH HHS R03 AI095040
6 · The paper itself

Abstract

Apoptosis of uninfected bystander cells is a key element of HIV pathogenesis and believed to be the driving force behind the selective depletion of CD4+ T cells leading to immunodeficiency. While several viral proteins have been implicated in this process the complex interaction between Env glycoprotein expressed on the surface of infected cells and the receptor and co-receptor expressing bystander cells has been proposed as a major mechanism. HIV-1 utilizes CD4 as the primary receptor for entry into cells; however, it is the viral co-receptor usage that greatly influences CD4 decline and progression to AIDS. This phenomenon is relatively simple for X4 viruses, which arise later during the course of the disease, are considered to be highly fusogenic, and cause a rapid CD4+ T cell decline. However, in contrast, R5 viruses in general have a greater transmissibility, are encountered early during the disease and have a lesser pathogenic potential than the former. The above generalization gets complicated in numerous situations where R5 viruses persist throughout the disease and are capable of causing a rigorous CD4+ T cell decline. This review will discuss the multiple factors that are reported to influence HIV induced bystander apoptosis and pathogenesis including Env glycoprotein phenotype, virus tropism, disease stage, co-receptor expression on CD4+ T cells, immune activation and therapies targeting the viral envelope.

Indexed as

AnimalsApoptosisAutophagyBystander EffectDisease Models, AnimalDisease Progressionenv Gene Products, Human Immunodeficiency VirusHIV-1HIV Envelope Protein gp41HIV InfectionsHumansMembrane FusionReceptors, CCR5Receptors, CXCR4env Gene Products, Human Immunodeficiency VirusHIV Envelope Protein gp41Receptors, CCR5Receptors, CXCR4

Identifiers

PMID23202514
PMCPMC3509682
OpenAlexW1985050346

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.