Evidence map›Paper›PMID 35283191›Full record

ArticleThe Journal of biological chemistry2022

Antigenic analysis of the HIV-1 envelope trimer implies small differences between structural states 1 and 2.

Evan M Cale, Jefferson I Driscoll, Myungjin Lee, Jason Gorman, Tongqing Zhou, Maolin Lu, Hui Geng, Yen-Ting Lai, Gwo-Yu Chuang, Nicole A Doria-Rose and 3 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Evan M CaleVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Jefferson I DriscollVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Myungjin LeeVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Jason GormanVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Tongqing ZhouVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Maolin LuDepartment of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA; Department of Cellular and Molecular Biology, University of Texas Health Science Center, Tyler, Texas, USA.
Hui GengVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Yen-Ting LaiVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Gwo-Yu ChuangVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Nicole A Doria-RoseVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Walther MothesDepartment of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Peter D KwongVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: pdkwong@nih.gov.
John R MascolaVaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: jmascola@mail.nih.gov.
National Institutes of Health · USYale University · US

Funding

Mechanisms Of Humoral EvasionZIAAI005023 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ZHOU, TONGQING · 2009 to 2025
$18.6M
Isolation of Monoclonal Antiobodies Against HIVZIAAI005095 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DORIA-ROSE, NICOLE · 2009 to 2025
$14.5M
Understanding Envelope Function in HIV-1 Infection: The Design, Synthesis and Validation of Small Molecule HIV-1 Env InhibitorsP01AI150471 · NIAID · DREXEL UNIVERSITY · PI HENDRICKSON, WAYNE A. · 2019 to 2022
$7.8M
HIV-1 Env structure and function assessed by parallel smFRET and cryoETR01AI150560 · NIAID · YALE UNIVERSITY · PI BLANCHARD, SCOTT C, LIU, JUN · 2019 to 2022
$3.4M
HIV-1 Env protein structure and function assessed by parallel smFRET and cryoETR37AI150560 · NIAID · YALE UNIVERSITY · PI WALTHER H MOTHES · 2023 to 2026
$3.2M
NIAID NIH HHS P01 AI150471NIAID NIH HHS R01 AI150560NIAID NIH HHS R37 AI150560
6 · The paper itself

Abstract

The conformationally dynamic HIV-1 envelope trimer (Env) is the target of broadly neutralizing antibodies (bnAbs) that block viral entry. Single-molecule Förster resonance energy transfer (smFRET) has revealed that HIV-1 Env exists in at least three conformational states on the virion. Prior to complete host-receptor engagement (State 3), Env resides most prevalently in the smFRET-defined State 1, which is preferentially recognized by most bnAbs that are elicited by natural infection. smFRET has also revealed that soluble trimers containing prefusion-stabilizing disulfide and isoleucine-to-proline substitutions reside primarily in State 2, which is a required intermediate between States 1 and 3. While high-resolution Env structures have been determined for States 2 and 3, the structure of these trimers in State 1 is unknown. To provide insight into the State 1 structure, here we characterized antigenic differences between smFRET-defined states and then correlated these differences with known structural differences between States 2 and 3. We found that cell surface-expressed Env was enriched in each state using state-enriching antibody fragments or small-molecule virus entry inhibitors and then assessed binding to HIV-1 bnAbs preferentially binding different states. We observed small but consistent differences in binding between Env enriched in States 1 and 2, and a more than 10-fold difference in binding to Env enriched in these states versus Env enriched in State 3. We conclude that structural differences between HIV-1 Env States 1 and 3 are likely more than 10-fold greater than those between States 1 and 2, providing important insight into State 1.

Indexed as

env Gene Products, Human Immunodeficiency VirusHIV-1HIV InfectionsBroadly Neutralizing AntibodiesHIV AntibodiesHumansProtein ConformationBroadly Neutralizing Antibodiesenv Gene Products, Human Immunodeficiency VirusHIV Antibodiesbroadly neutralizing antibodyconformational changeflow cytometryglycoprotein structureHIV-1intermediate conformationssmFRETSOSIP

Identifiers

PMID35283191
PMCPMC9006658
OpenAlexW4220978810

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Registered trials

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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.