Evidence map›Paper›PMID 22145853›Full record

ArticleRetrovirology2011

Inhibition of HIV-1 endocytosis allows lipid mixing at the plasma membrane, but not complete fusion.

Michelle de la Vega, Mariana Marin, Naoyuki Kondo, Kosuke Miyauchi, Yuri Kim, Raquel F Epand, Richard M Epand, Gregory B Melikyan

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  4. Macropinosomes are a site of HIV-1 entry into primary CD4Proceedings of the National Academy of Sciences of the United States of America · 2025
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17 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

8 authors at 4 institutions in 3 countries.

Michelle de la VegaDivision of Pediatric Infectious Diseases, Emory University Children's Center, 2015 Uppergate Drive, Atlanta, GA 30322, USA.
Mariana Marin
Naoyuki Kondo
Kosuke Miyauchi
Yuri Kim
Raquel F Epand
Richard M Epand
Gregory B Melikyan
Children's Center · USHealth Sciences Centre · CAEmory University · USRIKEN Center for Integrative Medical Sciences · JP

Funding

BIOPHYSICS OF PROTEIN-MEDIATED MEMBRANE FUSIONR01GM054787 · NIGMS · UNIVERSITY OF MD BIOTECHNOLOGY INSTITUTE · PI MELIKIAN, GREGORY B · 2000 to 2018
$6.5M
CIHR MOP 86608NIGMS NIH HHS R01 GM054787
6 · The paper itself

Abstract

backgroundWe recently provided evidence that HIV-1 enters HeLa-derived TZM-bl and lymphoid CEMss cells by fusing with endosomes, whereas its fusion with the plasma membrane does not proceed beyond the lipid mixing step. The mechanism of restriction of HIV-1 fusion at the cell surface and/or the factors that aid the virus entry from endosomes remain unclear.

resultsWe examined HIV-1 fusion with a panel of target cells lines and with primary CD4+ T cells. Kinetic measurements of fusion combined with time-resolved imaging of single viruses further reinforced the notion that HIV-1 enters the cells via endocytosis and fusion with endosomes. Furthermore, we attempted to deliberately redirect virus fusion to the plasma membrane, using two experimental strategies. First, the fusion reaction was synchronized by pre-incubating the viruses with cells at reduced temperature to allow CD4 and coreceptors engagement, but not the virus uptake or fusion. Subsequent shift to a physiological temperature triggered accelerated virus uptake followed by entry from endosomes, but did not permit fusion at the cell surface. Second, blocking HIV-1 endocytosis by a small-molecule dynamin inhibitor, dynasore, resulted in transfer of viral lipids to the plasma membrane without any detectable release of the viral content into the cytosol. We also found that a higher concentration of dynasore is required to block the HIV-endosome fusion compared to virus internalization.

conclusionsOur results further support the notion that HIV-1 enters disparate cell types through fusion with endosomes. The block of HIV-1 fusion with the plasma membrane at a post-lipid mixing stage shows that this membrane is not conducive to fusion pore formation and/or enlargement. The ability of dynasore to interfere with the virus-endosome fusion suggests that dynamin could be involved in two distinct steps of HIV-1 entry - endocytosis and fusion within intracellular compartments.

Indexed as

EndocytosisVirus InternalizationCD4-Positive T-LymphocytesCell MembraneCytoplasmEndosomesFluorescent DyesHeLa CellsHIV-1HIV InfectionsHumansHydrazonesMembrane LipidsVirus ReleaseFluorescent DyesHydrazonesMembrane LipidsN'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide

Identifiers

PMID22145853
PMCPMC3297528
OpenAlexW2026939674

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.