Evidence map›Paper›PMID 27343732›Full record

ArticleVirology2016

HIV-1 Vpr increases Env expression by preventing Env from endoplasmic reticulum-associated protein degradation (ERAD).

Xianfeng Zhang, Tao Zhou, Dylan A Frabutt, Yong-Hui Zheng

Abstract read
In one paragraph

Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
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  4. Viruses Hijack ERAD to Regulate Their Replication and Propagation.International journal of molecular sciences · 2022
    Review
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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

4 authors at 2 institutions in 2 countries.

Xianfeng ZhangHarbin Veterinary Research Institute, CAAS-Michigan State University Joint Laboratory of Innate Immunity, State Key Laboratory of Veterinary Biotechnology, Chinese Academy of Agricultural Sciences, Harbin 150001, China; Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA.
Tao ZhouHarbin Veterinary Research Institute, CAAS-Michigan State University Joint Laboratory of Innate Immunity, State Key Laboratory of Veterinary Biotechnology, Chinese Academy of Agricultural Sciences, Harbin 150001, China; Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA.
Dylan A FrabuttDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA.
Yong-Hui ZhengHarbin Veterinary Research Institute, CAAS-Michigan State University Joint Laboratory of Innate Immunity, State Key Laboratory of Veterinary Biotechnology, Chinese Academy of Agricultural Sciences, Harbin 150001, China; Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA. Electronic address: zhengyo@msu.edu.
Chinese Academy of Agricultural Sciences · CNMichigan State University · US

Funding

To eradicate the HIV macrophage reservoirR01AI120189 · NIAID · MICHIGAN STATE UNIVERSITY · PI ZHENG, YONG-HUI · 2015 to 2017
$589k
VprR21AI106477 · NIAID · MICHIGAN STATE UNIVERSITY · PI ZHENG, YONG-HUI · 2013 to 2014
$408k
NIAID NIH HHS R01 AI120189NIAID NIH HHS R21 AI106477
6 · The paper itself

Abstract

Vpr enhances HIV-1 replication in macrophages and dendritic cells, as well as the human CD4(+) CEM.NKR T cell line. Recently, Vpr was reported to increase HIV-1 Env expression in macrophages. Here, we report that Vpr also increases HIV-1 Env expression in dendritic cells and CEM.NKR cells. The Vpr activity depends on its N-terminal region, which was disrupted by a single A30L mutation. Env was rapidly degraded in the absence of Vpr, which was blocked by the ERAD pathway inhibitor kifunesine or the lysosome inhibitor Bafilomycin. As2O3 or PK11195, which reportedly enhances HIV-1 Env folding, also blocked the Env degradation in CEM.NKR cells. Thus, these results not only identify Env as a primary target for Vpr to boost HIV-1 replication, but also suggest that Vpr likely promotes Env folding in the ER, which is otherwise misfolded and targeted by the ERAD pathway to lysosomes for degradation.

Indexed as

Endoplasmic Reticulum-Associated DegradationGene Expression Regulation, ViralAnimalsCell LineEndoplasmic Reticulumenv Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsHumansProteolysisVirus Replicationvpr Gene Products, Human Immunodeficiency Virusenv Gene Products, Human Immunodeficiency Virusvpr Gene Products, Human Immunodeficiency VirusEndoplasmic reticulum-associated protein degradation (ERAD)GlycoproteinHuman immunodeficiency virus (HIV)Protein degradationViral proteinVpr

Identifiers

PMID27343732
PMCPMC4969109
OpenAlexW2470238170

What OpenQuestion holds

Textmetadata
LicenceTDM
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.