Evidence map›Paper›PMID 27199430›Full record

ArticleScience (New York, N.Y.)2016

Enhanced clearance of HIV-1-infected cells by broadly neutralizing antibodies against HIV-1 in vivo.

Ching-Lan Lu, Dariusz K Murakowski, Stylianos Bournazos, Till Schoofs, Debolina Sarkar, Ariel Halper-Stromberg, Joshua A Horwitz, Lilian Nogueira, Jovana Golijanin, Anna Gazumyan and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 2 pooled it
26.8field-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

252 citing papers in PubMed, 2 syntheses or guidelines pooled it, 346 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 1 country.

Ching-Lan LuLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA.
Dariusz K MurakowskiDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Stylianos BournazosLaboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10065, USA.
Till SchoofsLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Debolina SarkarDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Ariel Halper-StrombergLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Joshua A HorwitzLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Lilian NogueiraLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Jovana GolijaninLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Anna GazumyanLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Jeffrey V RavetchLaboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10065, USA.
Marina CaskeyLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Arup K ChakrabortyDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA. Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. nussen@rockefeller.edu arupc@mit.edu.
Michel C NussenzweigLaboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA. Howard Hughes Medical Institute. nussen@rockefeller.edu arupc@mit.edu.
Rockefeller University · USMassachusetts Institute of Technology · USCornell University · USHoward Hughes Medical Institute · USRagon Institute of MGH, MIT and Harvard · US

Funding

Support Component D/Vaccine Discovery, Concept to ClinicUM1AI100663 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GODZIK, ADAM · 2012 to 2018
$131.5M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Stuctural basis of bNab activityP01AI100148 · NIAID · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI Pamela J Bjorkman · 2013 to 2026
$43.3M
Transforming Translational Science and Education to Benefit Human HealthUL1TR000043 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2012 to 2015
$26.8M
Protein Expression CoreP01AI081677 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 2009 to 2013
$10.6M
Cellular and molecular dissection of HIV-1 latency in vivoF31AI118555 · NIAID · ROCKEFELLER UNIVERSITY · PI HORWITZ, JOSHUA A · 2015 to 2016
$62k
Howard Hughes Medical InstituteNCATS NIH HHS 8 UL1 TR000043NCATS NIH HHS UL1 TR000043NIAID NIH HHS 1UM1 AI100663-01NIAID NIH HHS AI081677-05NIAID NIH HHS AI100148-02NIAID NIH HHS F31 AI118555NIAID NIH HHS F31 AI118555-01NIAID NIH HHS P01 AI081677NIAID NIH HHS P01 AI100148NIAID NIH HHS UM1 AI100663NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Antiretroviral drugs and antibodies limit HIV-1 infection by interfering with the viral life cycle. In addition, antibodies also have the potential to guide host immune effector cells to kill HIV-1-infected cells. Examination of the kinetics of HIV-1 suppression in infected individuals by passively administered 3BNC117, a broadly neutralizing antibody, suggested that the effects of the antibody are not limited to free viral clearance and blocking new infection but also include acceleration of infected cell clearance. Consistent with these observations, we find that broadly neutralizing antibodies can target CD4(+) T cells infected with patient viruses and can decrease their in vivo half-lives by a mechanism that requires Fcγ receptor engagement in a humanized mouse model. The results indicate that passive immunotherapy can accelerate elimination of HIV-1-infected cells.

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingApoptosisBroadly Neutralizing AntibodiesCD4-Positive T-LymphocytesCell LineHIV-1HIV AntibodiesHIV InfectionsHomeodomain ProteinsHumansImmunization, PassiveImmunosuppression TherapyInterleukin Receptor Common gamma SubunitMice3BNC117 antibodyAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingBroadly Neutralizing AntibodiesHIV AntibodiesHomeodomain ProteinsIl2rg protein, mouseInterleukin Receptor Common gamma SubunitRAG-1 proteinReceptors, IgG

Identifiers

PMID27199430
PMCPMC5126967
OpenAlexW2347047438

What OpenQuestion holds

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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.