Evidence map›Paper›PMID 16764724›Full record

ArticleRetrovirology2006

Interactions between Nef and AIP1 proliferate multivesicular bodies and facilitate egress of HIV-1.

Luciana J Costa, Nan Chen, Adriana Lopes, Renato S Aguiar, Amilcar Tanuri, Ana Plemenitas, B Matija Peterlin

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016
    Pooled it
  2. Review
  3. Article
  4. Role of Monocyte/Macrophages in the Pathogenesis of NeuroHIV.Results and problems in cell differentiation · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

7 authors at 3 institutions in 3 countries.

Luciana J CostaMolecular Virology Laboratory, Dep. of Genetics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. ljcosta@biologia.ufrj.br
Nan Chen
Adriana Lopes
Renato S Aguiar
Amilcar Tanuri
Ana Plemenitas
B Matija Peterlin
Universidade Federal do Rio de Janeiro · BRUniversity of California, San Francisco · USUniversity of Ljubljana · SI

Funding

Mechanism of HIV 1 Nef ActionR01AI051165 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PETERLIN, BORIS MATIJA · 2002 to 2006
$1.9M
NIAID NIH HHS R01 AI051165
6 · The paper itself

Abstract

backgroundNef is an accessory protein of primate lentiviruses, HIV-1, HIV-2 and SIV. Besides removing CD4 and MHC class I from the surface and activating cellular signaling cascades, Nef also binds GagPol during late stages of the viral replicative cycle. In this report, we investigated further the ability of Nef to facilitate the replication of HIV-1.

resultsTo this end, first the release of new viral particles was much lower in the absence of Nef in a T cell line. Since the same results were obtained in the absence of the viral envelope using pseudo-typed viruses, this phenomenon was independent of CD4 and enhanced infectivity. Next, we found that Nef not only possesses a consensus motif for but also binds AIP1 in vitro and in vivo. AIP1 is the critical intermediate in the formation of multivesicular bodies (MVBs), which play an important role in the budding and release of viruses from infected cells. Indeed, Nef proliferated MVBs in cells, but only when its AIP1-binding site was intact. Finally, these functions of Nef were reproduced in primary macrophages, where the wild type but not mutant Nef proteins led to increased release of new viral particles from infected cells.

conclusionWe conclude that by binding GagPol and AIP1, Nef not only proliferates MVBs but also contributes to the egress of viral particles from infected cells.

Indexed as

Adaptor Proteins, Signal TransducingAmino Acid SequenceBinding SitesCarrier ProteinsCD4 AntigensCell Line, TransformedConsensus SequenceGene Products, gagGene Products, nefGuanylate KinasesHIV-1HumansMacrophagesMolecular Sequence Datanef Gene Products, Human Immunodeficiency VirusProteinsAdaptor Proteins, Signal TransducingCarrier ProteinsCD4 AntigensGene Products, gagGene Products, nefGuanylate KinasesMAGI2 protein, humannef Gene Products, Human Immunodeficiency VirusProteins

Identifiers

PMID16764724
PMCPMC1526754
OpenAlexW2110141748

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.