Evidence map›Paper›PMID 28842659›Full record

ArticleScientific reports2017

HIV-1 envelope glycoprotein stimulates viral transcription and increases the infectivity of the progeny virus through the manipulation of cellular machinery.

Xiaozhuo Ran, Zhujun Ao, Adriana Trajtman, Wayne Xu, Gary Kobinger, Yoav Keynan, Xiaojian Yao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  5. Biomedical engineering and computational biology · 2023
    Article
  6. Complex Relationships between HIV-1 Integrase and Its Cellular Partners.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
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  12. 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

7 authors at 4 institutions in 2 countries.

Xiaozhuo RanLaboratory of Molecular Human Retrovirology, University of Manitoba, Winnipeg, MB, Canada.
Zhujun AoLaboratory of Molecular Human Retrovirology, University of Manitoba, Winnipeg, MB, Canada.
Adriana TrajtmanDepartment of Medical Microbiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Wayne XuResearch Institute in Oncology and Hematology, CancerCare Manitoba, Winnipeg, MB, Canada.
Gary KobingerCentre de Recherche en Infectiologie de l'Université Laval/Centre Hospitalier de l'Université Laval (CHUL), Québec, QC, Canada.
Yoav KeynanDepartment of Medical Microbiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Xiaojian YaoLaboratory of Molecular Human Retrovirology, University of Manitoba, Winnipeg, MB, Canada. xiao-jian.yao@umanitoba.ca.
University of Manitoba · CACentral South University · CNCentre hospitalier de l'Université Laval · CAResearch Institute in Oncology and Hematology · CA

Funding

CIHR HBF-131553
6 · The paper itself

Abstract

During HIV infection, large amounts of progeny viral particles, including infectious virus and a large proportion of defective viral particles, are produced. Despite of the critical role of the infectious viruses in infection and pathogenesis in vivo, whether and how those defective viral particles, especially the virus-associated envelope glycoprotein (vEnv), would impact viral infection remains elusive. In this study, we investigated the effect of vEnv on HIV-infected T cells and demonstrated that the vEnv was able to stimulate HIV transcription in HIV-infected cells, including peripheral blood mononuclear cells (PBMCs) isolated from HIV patients. This vEnv-mediated HIV transcription activation is mediated primarily through the interaction between vEnv and CD4/coreceptors (CCR5 or CXCR4). Through transcriptome analysis, we found that numerous cellular gene products involved in various signaling pathways were modulated by vEnv. Among them, we have further identified a cellular microRNA miR181A2, which is downregulated upon vEnv treatment, resulting in increased HIV LTR histone H3 acetylation and HIV transcription. Furthermore, we also found a vEnv-modulated cellular histone deacetylase, HDAC10, whose downregulation is associated with the increased infectivity of progeny viruses. Altogether, these findings provide evidence of the important role vEnv plays in modulating cellular environments and facilitating HIV expression and infection.

Indexed as

Gene Expression Regulation, ViralHost-Pathogen InteractionsTranscription, GeneticVirus ReplicationCD4 AntigensCD4-Positive T-Lymphocytesenv Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHIV Long Terminal RepeatHumansLeukocytes, MononuclearProtein BindingReceptors, CCR5Receptors, CXCR4Signal TransductionCCR5 protein, humanCD4 AntigensCXCR4 protein, humanenv Gene Products, Human Immunodeficiency VirusReceptors, CCR5Receptors, CXCR4

Identifiers

PMID28842659
PMCPMC5573355
OpenAlexW2746704685

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.