Evidence map›Paper›PMID 26764036›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

HIV-1 Env Glycoprotein Phenotype along with Immune Activation Determines CD4 T Cell Loss in HIV Patients.

Anjali Joshi, Melina Sedano, Bethany Beauchamp, Erin B Punke, Zuber D Mulla, Armando Meza, Ogechika K Alozie, Debabrata Mukherjee, Himanshu Garg

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 26 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

9 authors at 1 institution in 1 country.

Anjali JoshiCenter of Excellence for Infectious Diseases, Department of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX 79905;
Melina SedanoCenter of Excellence for Infectious Diseases, Department of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX 79905;
Bethany BeauchampPaul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX 79905;
Erin B PunkeCenter of Excellence for Infectious Diseases, Department of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX 79905;
Zuber D MullaDepartment of Obstetrics and Gynecology, Texas Tech University Health Sciences Center, El Paso, TX 79905; and.
Armando MezaDepartment of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX 79905.
Ogechika K AlozieDepartment of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX 79905.
Debabrata MukherjeeDepartment of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX 79905.
Himanshu GargCenter of Excellence for Infectious Diseases, Department of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX 79905; himanshu.garg@ttuhsc.edu.ORCID http://orcid.org/0000-0001-8906-9300
Texas Tech University · US

Funding

Host and Viral Factors in HIV Pathogenesis.R15AI116240 · NIAID · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI GARG, HIMANSHU · 2015 to 2015
$383k
NIAID NIH HHS R15 AI116240NIAID NIH HHS R15 AI116240-01A1
6 · The paper itself

Abstract

The mechanism behind the selective depletion of CD4(+) cells in HIV infections remains undetermined. Although HIV selectively infects CD4(+) cells, the relatively few infected cells in vivo cannot account for the extent of CD4(+) T cell depletion, suggesting indirect or bystander mechanisms. The role of virus replication, Env glycoprotein phenotype, and immune activation (IA) in this bystander phenomenon remains controversial. Using samples derived from HIV-infected patients, we demonstrate that, although IA in both CD4(+) and CD8(+) subsets correlates with CD4 decline, apoptosis in CD4(+) and not CD8(+) cells is associated with disease progression. Because HIV-1 Env glycoprotein has been implicated in bystander apoptosis, we cloned full-length Envs from plasma of viremic patients and tested their apoptosis-inducing potential (AIP). Interestingly, AIP of HIV-1 Env glycoproteins were found to correlate inversely with CD4:CD8 ratios, suggesting a role of Env phenotype in disease progression. In vitro mitogenic stimulation of PBMCs resulted in upregulation of IA markers but failed to alter the CD4:CD8 ratio. However, coculture of normal PBMCs with Env-expressing cells resulted in selective CD4 loss that was significantly enhanced by IA. Our study demonstrates that AIP of HIV-1 Env and IA collectively determine CD4 loss in HIV infection.

Indexed as

CD4-CD8 RatioAdultApoptosisCD4-Positive T-LymphocytesFemaleGene Products, envHIV-1HIV InfectionsHumansMalePhenotypeGene Products, env

Identifiers

PMID26764036
PMCPMC4744550
OpenAlexW2235523204

What OpenQuestion holds

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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.