Evidence map›Paper›PMID 26474824›Full record

ArticleThe Journal of general virology2016

Lentiviral hepatitis B pseudotype entry requires sodium taurocholate co-transporting polypeptide and additional hepatocyte-specific factors.

L W Meredith, K Hu, X Cheng, C R Howard, T F Baumert, P Balfe, K F van de Graaf, U Protzer, J A McKeating

Open access · hybridAbstract read
In one paragraph

Article in The Journal of general virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Concentration of NaScientific reports · 2021
    Article
  2. Review
  3. Article
  4. Defined host factors support HBV infection in non-hepatic 293T cells.Journal of cellular and molecular medicine · 2020
    Article
  5. Article
  6. Epidermal growth factor receptor is a host-entry cofactor triggering hepatitis B virus internalization.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Review
  8. Article
  9. Article
  10. Review
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

9 authors at 4 institutions in 3 countries.

L W MeredithCentre for Human Virology, Viral Hepatitis Laboratory, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
K HuCentre for Human Virology, Viral Hepatitis Laboratory, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
X ChengInstitute of Virology, Technische Universität München/Helmholtz Zentrum München, Munich, Germany.
C R HowardCentre for Human Virology, Viral Hepatitis Laboratory, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
T F BaumertINSERM U1110, Institut de Recherche sur les Maladies Virales et Hépatiques and Université de Strasbourg, Strasbourg, France.
P BalfeCentre for Human Virology, Viral Hepatitis Laboratory, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
K F van de GraafTytgat Institute for Liver and Intestinal Research and Department of Gastroenterology and Hepatology, AMC, Amsterdam, The Netherlands.
U ProtzerInstitute of Virology, Technische Universität München/Helmholtz Zentrum München, Munich, Germany.
J A McKeatingInstitute for Advanced Study, Technische Universität München, Garching, Germany.
University of Birmingham · GBHelmholtz Zentrum München · DEInserm · FRInstitute for Advanced Study · DE

Funding

European Research Council 337479Medical Research Council G0400802Medical Research Council G0801976Medical Research Council G1100247
6 · The paper itself

Abstract

Hepatitis B virus (HBV) is one of the world's major unconquered infections, resulting in progressive liver disease, and current treatments rarely cure infection. A limitation to discovering new therapies is our limited knowledge of HBV entry and dissemination pathways that hinders the development of in vitro culture systems. To address this gap in our understanding we optimized the genesis of infectious lentiviral pseudoparticles (HBVpps). The recent discovery that the bile salt transporter sodium taurocholate co-transporting polypeptide (NTCP) acts as a receptor for HBV enabled us to assess the receptor dependency of HBVpp infection. HBVpps preferentially infect hepatoma cells expressing NTCP, whereas other non-liver cells engineered to express NTCP do not support infection, suggesting that additional hepatocyte-specific factors are required for HBVpp internalization. These results highlight the value of the HBVpp system to dissect the pathways of HBV entry and dissemination.

Indexed as

Host-Pathogen InteractionsVirus InternalizationCell LineHepatitis B virusHepatocytesHumansLentivirusOrganic Anion Transporters, Sodium-DependentReceptors, VirusSymportersOrganic Anion Transporters, Sodium-DependentReceptors, Virussodium-bile acid cotransporterSymporters

Identifiers

PMID26474824
PMCPMC4772705
OpenAlexW2116812306

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.