Evidence map›Paper›PMID 30932366›Full record

ArticleJournal of the International AIDS Society2019

HIV-1 exposure and immune activation enhance sexual transmission of Hepatitis C virus by primary Langerhans cells.

Bernadien M Nijmeijer, Ramin Sarrami-Forooshani, Gaby S Steba, Renée Rce Schreurs, Sylvie M Koekkoek, Richard Molenkamp, Janke Schinkel, Peter Reiss, Matthijs L Siegenbeek van Heukelom, Marc van der Valk and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the International AIDS Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. 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 2 institutions in 1 country.

Bernadien M NijmeijerDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Ramin Sarrami-ForooshaniDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Gaby S StebaDepartment of Medical Microbiology, Clinical Virology Laboratory, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Renée Rce SchreursDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Sylvie M KoekkoekDepartment of Medical Microbiology, Clinical Virology Laboratory, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Richard MolenkampDepartment of Medical Microbiology, Clinical Virology Laboratory, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Janke SchinkelDepartment of Medical Microbiology, Clinical Virology Laboratory, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Peter ReissDepartment of Global Health, Amsterdam University Medical Centers, and Amsterdam Institute for Global Health and Development, Amsterdam University Medical Centers HIV Monitoring Foundation, Amsterdam, The Netherlands.
Matthijs L Siegenbeek van HeukelomDivision of Infectious Diseases, Department of Internal Medicine, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Marc van der ValkDivision of Infectious Diseases, Department of Internal Medicine, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Carla Ms RibeiroDepartment of Experimental Immunology, Amsterdam Infection and Immunity Institute, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0002-5682-4143
Teunis Bh 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 · NLAmsterdam Institute for Global Health and Development · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe significant rise in incidence of Hepatitis C virus (HCV) infection among men-who-have-sex-with-men (MSM) living with HIV-1 suggests that HCV under specific circumstances is transmitted via sexual contact. During sexual transmission HCV has to cross the epithelial barrier to either directly enter the blood stream or indirectly via mucosal immune cells. However, the mechanisms of sexual transmission of HCV remain unclear. We investigated the role of Langerhans cells (LCs) in HCV susceptibility during sexual contact as LCs are among the first cells in mucosal tissues to encounter invading viruses.

methodsWe investigated the phenotype of primary LCs in anal biopsies from MSM living with HIV-1. To investigate the role of primary LCs in HCV infection and transmission, we have used both isolated primary skin LCs and the ex vivo tissue transmission model.

resultsOur data identified an important role for mucosal LCs in facilitating HCV transmission after HIV-1 exposure or immune activation. LCs were detected within mucosal anal tissues obtained from HIV-1 positive MSM biopsies. In order to perform functional studies, we used primary LCs from skin, which have a similar phenotype as mucosal LCs. Immature LCs were neither infected nor transmitted HCV to hepatocytes. Notably, exposure to HIV-1 significantly increased HCV transmission by LCs in the ex vivo transmission model. HIV-1 replication was crucial for the increased HCV transmission as HIV-1 inhibitors significantly reduced HIV-1-induced HCV transmission. Moreover, tissue immune activation of LCs also increased HCV transmission to target cells.

conclusionsThus, our data strongly indicate that HIV-1 or immune activation in MSM leads to capture of HCV by mucosal LCs, which might facilitate transmission to other cells or allow entry of HCV into the blood. This novel transmission mechanism by LCs also implicates that the activation state of LCs is an important cellular determinant for HCV susceptibility after sexual contact.

Indexed as

AdultCells, CulturedHepacivirusHepatitis CHIV-1HIV InfectionsHumansLangerhans CellsMaleMucous MembraneSexually Transmitted DiseasesHepatitis C virusHIV-1Immune activationLangerhans CellsMen-who-have-Sex-with-MenViral transmission

Identifiers

PMID30932366
PMCPMC6442005
OpenAlexW2930388206

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.