Evidence map›Paper›PMID 23637402›Full record

ArticleJournal of virology2013

Clustering and mobility of HIV-1 Env at viral assembly sites predict its propensity to induce cell-cell fusion.

Nathan H Roy, Jany Chan, Marie Lambelé, Markus Thali

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.8field-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

73 citing papers in PubMed, 94 citations in OpenAlex.

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13 more citing papers are in PubMed but not listed here.

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.

Nathan H RoyGraduate Program in Cell and Molecular Biology, University of Vermont, Burlington, Vermont, USA.
Jany Chan
Marie Lambelé
Markus Thali
University of Vermont · US

Funding

Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Vermont Immunology/Infectious Diseases Training GrantT32AI055402 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI GARY E WARD · 2005 to 2026
$2.7M
Molecular regulation of HIV-1 assembly, release and cell-to-cell transmissionR01AI080302 · NIAID · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI THALI, MARKUS · 2009 to 2013
$1.9M
NIAID NIH HHS R01 AI080302NIAID NIH HHS T32 AI055402NIAID NIH HHS T32 AI055402-06A1
6 · The paper itself

Abstract

HIV-1 Env mediates virus attachment to and fusion with target cell membranes, and yet, while Env is still situated at the plasma membrane of the producer cell and before its incorporation into newly formed particles, Env already interacts with the viral receptor CD4 on target cells, thus enabling the formation of transient cell contacts that facilitate the transmission of viral particles. During this first encounter with the receptor, Env must not induce membrane fusion, as this would prevent the producer cell and the target cell from separating upon virus transmission, but how Env's fusion activity is controlled remains unclear. To gain a better understanding of the Env regulation that precedes viral transmission, we examined the nanoscale organization of Env at the surface of producer cells. Utilizing superresolution microscopy (stochastic optical reconstruction microscopy [STORM]) and fluorescence recovery after photobleaching (FRAP), we quantitatively assessed the clustering and dynamics of Env upon its arrival at the plasma membrane. We found that Gag assembly induced the aggregation of small Env clusters into larger domains and that these domains were completely immobile. Truncation of the cytoplasmic tail (CT) of Env abrogated Gag's ability to induce Env clustering and restored Env mobility at assembly sites, both of which correlated with increased Env-induced fusion of infected and uninfected cells. Hence, while Env trapping by Gag secures Env incorporation into viral particles, Env clustering and its sequestration at assembly sites likely also leads to the repression of its fusion function, and thus, by preventing the formation of syncytia, Gag helps to secure efficient transfer of viral particles to target cells.

Indexed as

Virus AttachmentVirus InternalizationAnalysis of VarianceCell FusionFluorescence Recovery After PhotobleachingGene Products, gagHeLa CellsHIV Envelope Protein gp120HumansMicroscopyVirus AssemblyGene Products, gaggp120 protein, Human immunodeficiency virus 1HIV Envelope Protein gp120

Identifiers

PMID23637402
PMCPMC3700267
OpenAlexW2147614247

What OpenQuestion holds

Textmetadata
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.