Evidence map›Paper›PMID 26950141›Full record

ReviewViruses2016

Remodeling of the Host Cell Plasma Membrane by HIV-1 Nef and Vpu: A Strategy to Ensure Viral Fitness and Persistence.

Scott M Sugden, Mariana G Bego, Tram N Q Pham, Éric A Cohen

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. HIV-1 manipulates CD96 on CD4Science advances · 2025
    Article
  2. Article
  3. Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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  12. Article
  13. Article
  14. Review
  15. Article
  16. PSGL-1 restricts HIV-1 infectivity by blocking virus particle attachment to target cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Loss of Nef-mediated CD3 down-regulation in the HIV-1 lineage increases viral infectivity and spread.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

4 authors at 1 institution in 1 country.

Scott M SugdenLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal (IRCM), 110 Pine Avenue West, Montreal, QC H2W 1R7, Canada. scott.sugden@ircm.qc.ca.
Mariana G BegoLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal (IRCM), 110 Pine Avenue West, Montreal, QC H2W 1R7, Canada. mariana.bego@ircm.qc.ca.
Tram N Q PhamLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal (IRCM), 110 Pine Avenue West, Montreal, QC H2W 1R7, Canada. tram.pham@ircm.qc.ca.
Éric A CohenLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal (IRCM), 110 Pine Avenue West, Montreal, QC H2W 1R7, Canada. eric.cohen@ircm.qc.ca.
Montreal Clinical Research Institute · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

The plasma membrane protects the cell from its surroundings and regulates cellular communication, homing, and metabolism. Not surprisingly, the composition of this membrane is highly controlled through the vesicular trafficking of proteins to and from the cell surface. As intracellular pathogens, most viruses exploit the host plasma membrane to promote viral replication while avoiding immune detection. This is particularly true for the enveloped human immunodeficiency virus (HIV), which assembles and obtains its lipid shell directly at the plasma membrane. HIV-1 encodes two proteins, negative factor (Nef) and viral protein U (Vpu), which function primarily by altering the quantity and localization of cell surface molecules to increase virus fitness despite host antiviral immune responses. These proteins are expressed at different stages in the HIV-1 life cycle and employ a variety of mechanisms to target both unique and redundant surface proteins, including the viral receptor CD4, host restriction factors, immunoreceptors, homing molecules, tetraspanins and membrane transporters. In this review, we discuss recent progress in the study of the Nef and Vpu targeting of host membrane proteins with an emphasis on how remodeling of the cell membrane allows HIV-1 to avoid host antiviral immune responses leading to the establishment of systemic and persistent infection.

Indexed as

Host-Pathogen InteractionsCell MembraneHIV-1Human Immunodeficiency Virus ProteinsMembrane Proteinsnef Gene Products, Human Immunodeficiency VirusViral Regulatory and Accessory ProteinsViroporin ProteinsHuman Immunodeficiency Virus ProteinsMembrane Proteinsnef Gene Products, Human Immunodeficiency Virusnef protein, Human immunodeficiency virus 1Viral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1HIV-1host cell surface proteinsimmune evasionNefreplicationVpu

Identifiers

PMID26950141
PMCPMC4810257
OpenAlexW2291384654

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.