Evidence map›Paper›PMID 25339767›Full record

ArticleJournal of virology2015

The HIV-1 gp120 CD4-bound conformation is preferentially targeted by antibody-dependent cellular cytotoxicity-mediating antibodies in sera from HIV-1-infected individuals.

Maxime Veillette, Mathieu Coutu, Jonathan Richard, Laurie-Anne Batraville, Olina Dagher, Nicole Bernard, Cécile Tremblay, Daniel E Kaufmann, Michel Roger, Andrés Finzi

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
8.3field-weighted citation impact, top 1% 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

162 citing papers in PubMed, 215 citations in OpenAlex.

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  18. In vivo evolution of env in SHIV-AD8Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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102 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

10 authors at 3 institutions in 2 countries.

Maxime VeilletteCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Mathieu CoutuCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Jonathan RichardCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Laurie-Anne BatravilleCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Olina DagherCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada.
Nicole BernardDepartment of Experimental Medicine, McGill University, Montreal, Quebec, Canada.
Cécile TremblayCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Daniel E KaufmannCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Cambridge, Massachusetts, USA.
Michel RogerCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Andrés FinziCentre de Recherche du CHUM, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada andres.finzi@umontreal.ca.
Centre Hospitalier de l’Université de Montréal · CAUniversité de Montréal · CAMcGill University · CA

Funding

Canadian Institutes of Health Research 119334Canadian Institutes of Health Research 126630Canadian Institutes of Health Research 134117Canadian Institutes of Health Research 135349Canadian Institutes of Health Research 291485
6 · The paper itself

Abstract

unlabelledRecent studies have linked antibody Fc-mediated effector functions with protection or control of human immunodeficiency type 1 (HIV-1) and simian immunodeficiency (SIV) infections. Interestingly, the presence of antibodies with potent antibody-dependent cellular cytotoxicity (ADCC) activity in the Thai RV144 vaccine trial was suggested to correlate with decreased HIV-1 acquisition risk. These antibodies recently were found to recognize HIV envelope (Env) epitopes exposed upon Env-CD4 interaction. CD4 downregulation by Nef and Vpu, as well as Vpu-mediated BST-2 antagonism, were reported to modulate exposure of those CD4-induced HIV-1 Env epitopes and were proposed to play a role in reducing the susceptibility of infected cells to ADCC mediated by this class of antibodies. Here, we report the high prevalence of antibodies recognizing CD4-induced HIV-1 Env epitopes in sera from HIV-1-infected individuals, which correlated with their ability to mediate ADCC responses against HIV-1-infected cells, exposing these Env epitopes at the cell surface. Furthermore, our results indicate that Env variable regions V1, V2, V3, and V5 do not represent a major determinant for ADCC responses mediated by sera from HIV-1-infected individuals. Altogether, these findings suggest that HIV-1 tightly controls the exposure of certain Env epitopes at the surface of infected cells in order to prevent elimination by Fc-effector functions. IMPORTANCE: Here, we identified a particular conformation of HIV-1 Env that is specifically targeted by ADCC-mediating antibodies present in sera from HIV-1-infected individuals. This observation suggests that HIV-1 developed sophisticated mechanisms to minimize the exposure of these epitopes at the surface of infected cells.

Indexed as

Antibody-Dependent Cell CytotoxicityCD4 AntigensCohort StudiesEpitopesHIV-1HIV AntibodiesHIV Envelope Protein gp120HIV InfectionsHumansProtein BindingCD4 AntigensEpitopesgp120 protein, Human immunodeficiency virus 1HIV AntibodiesHIV Envelope Protein gp120

Identifiers

PMID25339767
PMCPMC4301108
OpenAlexW2035549114

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.