Evidence map›Paper›PMID 31856198›Full record

ArticlePloS one2019

Sexually transmitted founder HIV-1 viruses are relatively resistant to Langerhans cell-mediated restriction.

Nina Hertoghs, Bernadien M Nijmeijer, Nienke H van Teijlingen, Angharad E Fenton-May, Tanja M Kaptein, John L van Hamme, John C Kappes, Neeltje A Kootstra, Beatrice H Hahn, Persephone Borrow and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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  13. Innate Immune Response Against HIV-1.Advances in experimental medicine and biology · 2021
    Article
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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

12 authors at 4 institutions in 3 countries.

Nina HertoghsDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
Bernadien M NijmeijerDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
Nienke H van TeijlingenDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
Angharad E Fenton-MayNuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.
Tanja M KapteinDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
John L van HammeDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
John C KappesDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America.
Neeltje A KootstraDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
Beatrice H HahnDepartments of Medicine and Microbiology, University of Pennsylvania, Philadelphia, PA, United States of America.
Persephone BorrowNuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.
Carla M S RibeiroDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.
Teunis B H GeijtenbeekDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0002-5710-2839
Amsterdam University Medical Centers · NLUniversity of Oxford · GBUniversity of Alabama at Birmingham · USUniversity of Pennsylvania · US

Funding

Nonhuman primate studies for development of a prototype HIV vaccine that induces broadly neutralizing antibodiesUM1AI144371 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F. · 2019 to 2025
$190.4M
Virus and Antibody Gene Sequencing CoreP01AI131251 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Kevin Wiehe · 2017 to 2026
$40.7M
Restriction of HIV-1 transmission by type 1 interferonsR01AI114266 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HAHN, BEATRICE H · 2014 to 2018
$3.2M
Harnessing type 1 IFN-stimulated antiviral mechanisms for HIV vaccine designR01AI111789 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HAHN, BEATRICE H · 2014 to 2017
$816k
NIAID NIH HHS P01 AI131251NIAID NIH HHS R01 AI111789NIAID NIH HHS R01 AI114266NIAID NIH HHS UM1 AI144371
6 · The paper itself

Abstract

A single HIV-1 variant establishes infection of the host after sexual contact. Identifying the phenotypic characteristics of these Transmitted Founder (T/F) viruses is important to understand the restriction mechanisms during transmission. Langerhans cells (LCs) are the mucosal dendritic cell subset that has been shown to have a protective role in HIV-1 transmission. Immature LCs efficiently capture and degrade HIV-1 via langerin-mediated restriction. Here we have investigated the capacity of T/F HIV-1 strains to infect mucosal Langerhans cells (LCs). Notably, most T/F variants efficiently infected immature LCs derived from skin and vaginal tissue in contrast to chronic HIV-1 laboratory strains. Next we screened a panel of T/F viruses and their matched 6-month consensus sequence viruses. Interestingly most T/F variants infected immature LCs whereas donor-matched 6-month consensus sequence viruses had lost the ability to infect LCs. However, we also identified 6-month consensus sequence viruses that had retained an ability to infect LCs similar to that of the donor-matched T/F virus. Moreover, some T/F viruses and 6-month consensus sequence viruses were unable to infect immature LCs. Further analyses indicated that T/F viruses are less sensitive to langerin-mediated restriction. These data suggest that T/F HIV-1 variants have the ability to infect immature LCs, which will facilitate transmission.

Indexed as

Host-Pathogen InteractionsAntigens, CDCells, CulturedHEK293 CellsHIV-1HumansLangerhans CellsLectins, C-TypeMannose-Binding LectinsAntigens, CDCD207 protein, humanLectins, C-TypeMannose-Binding Lectins

Identifiers

PMID31856198
PMCPMC6922402
OpenAlexW2993703962

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.