Evidence map›Paper›PMID 22094081›Full record

ReviewAdvances in virus research2011

Human immunodeficiency virus viral protein R as an extracellular protein in neuropathogenesis.

Adriano Ferrucci, Michael R Nonnemacher, Brian Wigdahl

Open access · greenAbstract readReview
In one paragraph

Review in Advances in virus research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
2.3field-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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016
    Pooled it
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Intercellular Transport of Viral Proteins.Results and problems in cell differentiation · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Genetic variation and function of the HIV-1 Tat protein.Medical microbiology and immunology · 2019
    Review
  17. Review
  18. Article
  19. Article
  20. The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention.International journal of molecular sciences · 2017
    Review
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 1 institution in 1 country.

Adriano FerrucciSchool of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, Pennsylvania, USA.
Michael R Nonnemacher
Brian Wigdahl
Drexel University · US

Funding

High Specificity HIV-1 Markers Predictive of Neuro-AIDSR01DA019807 · NIDA · DREXEL UNIVERSITY · PI WIGDAHL, BRIAN · 2004 to 2014
$5.1M
NEUROLOGICAL &LYMPHOID FACTORS IN HIV1 LTR ACTIVATIONR01NS032092 · NINDS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI WIGDAHL, BRIAN · 1993 to 2011
$3.9M
NIDA NIH HHS DA19807NIDA NIH HHS R01 DA019807NINDS NIH HHS NS32092NINDS NIH HHS R01 NS032092
6 · The paper itself

Abstract

Numerous studies published in the past two decades have identified the viral protein R (Vpr) as one of the most versatile proteins in the life cycle of human immunodeficiency virus type 1 (HIV-1). In this regard, more than a thousand Vpr molecules are present in extracellular viral particles. Subsequent to viral entry, Vpr participates in early replicative events by assisting in viral genome nuclear import and, during the viral life cycle, by shuttling between the nucleus and the cytoplasm to accomplish its functions within the context of other replicative functions. Additionally, several studies have implicated Vpr as a proapoptotic protein because it promotes formation of permeability transition pores in mitochondria, which in turn affects transmembrane potential and adenosine triphosphate synthesis. Recent studies have identified Vpr as a virion-free protein in the serum and cerebrospinal fluid of patients infected with HIV-1 whose plasma viremia directly correlates with the extracellular concentration of Vpr. These observations pointed to a new role for Vpr as an additional weapon in the HIV-1 arsenal, involving the use of an extracellular protein to target and possibly inhibit HIV-1-uninfected bystander cells to enable them to escape immune surveillance. In addition, extracellular Vpr decreases adenosine triphosphate levels and affects the intracellular redox balance in neurons, ultimately causing their apoptosis. Herein, we review the role of Vpr as an extracellular protein and its downstream effects on cellular metabolism, functionality, and survival, with particular emphasis on how extracellular Vpr-induced oxidative stress might aggravate HIV-1-induced symptoms, thus affecting pathogenesis and disease progression.

Indexed as

ApoptosisHIV-1HumansNeuronsVirulence Factorsvpr Gene Products, Human Immunodeficiency VirusVirulence Factorsvpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID22094081
PMCPMC3731056
OpenAlexW1491801314

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.