Evidence map›Paper›PMID 19182773›Full record

ArticleNature2009

Human occludin is a hepatitis C virus entry factor required for infection of mouse cells.

Alexander Ploss, Matthew J Evans, Valeriya A Gaysinskaya, Maryline Panis, Hana You, Ype P de Jong, Charles M Rice

Open access · greenAbstract read
In one paragraph

Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 489 papers.

0numbers the graph read from it
0cells of the map it votes in
489citing papers in PubMed
48.8field-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

489 citing papers in PubMed, 908 citations in OpenAlex.

  1. Trial
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  8. Identification of claudin-3 as an entry factor for rat hepacivirus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  17. Phospholipid scramblase 1: a frontline defense against viral infections.Frontiers in cellular and infection microbiology · 2025
    Review
  18. Review
  19. Article
  20. Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Alexander PlossCenter for the Study of Hepatitis C, The Rockefeller University, New York, New York 10065, USA.
Matthew J Evans
Valeriya A Gaysinskaya
Maryline Panis
Hana You
Ype P de Jong
Charles M Rice
Rockefeller University · USIcahn School of Medicine at Mount Sinai · US

Funding

Identification and characterization of cellular factors involved in HCV entryR01AI072613 · NIAID · ROCKEFELLER UNIVERSITY · PI RICE, CHARLES M · 2007 to 2016
$4.7M
NIAID NIH HHS R01 AI072613
6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a leading cause of liver disease worldwide. The development of much needed specific antiviral therapies and an effective vaccine has been hampered by the lack of a convenient small animal model. The determinants restricting HCV tropism to human and chimpanzee hosts are unknown. Replication of the viral RNA has been demonstrated in mouse cells, but these cells are not infectable with either lentiviral particles bearing HCV glycoproteins (HCVpp) or HCV produced in cell culture (HCVcc) (A.P., M.E. and C.M.R., unpublished observations), suggesting that there is a block at the level of entry. Here we show, using an iterative complementary DNA library screening approach, that human occludin (OCLN) is an essential HCV cell entry factor that is able to render murine cells infectable with HCVpp. Similarly, OCLN is required for the HCV-susceptibility of human cells, because its overexpression in uninfectable cells specifically enhanced HCVpp uptake, whereas its silencing in permissive cells impaired both HCVpp and HCVcc infection. In addition to OCLN, HCVpp infection of murine cells required expression of the previously identified HCV entry factors CD81 (ref. 4), scavenger receptor class B type I (SR-BI, also known as SCARB1) and claudin-1 (CLDN1). Although the mouse versions of SR-BI and CLDN1 function at least as well as the human proteins in promoting HCV entry, both OCLN and CD81 must be of human origin to allow efficient infection. The species-specific determinants of OCLN were mapped to its second extracellular loop. The identification of OCLN as a new HCV entry factor further highlights the importance of the tight junction complex in the viral entry process, and provides an important advance towards efforts to develop small animal models for HCV.

Indexed as

Virus Internalization3T3 CellsAnimalsAntigens, CDCell LineCHO CellsCricetinaeCricetulusGene Expression RegulationHepacivirusHepatitis CHumansMembrane ProteinsMiceOccludinTetraspanin 28Antigens, CDCD81 protein, humanCd81 protein, mouseMembrane ProteinsOccludinOCLN protein, humanOcln protein, mouseTetraspanin 28

Identifiers

PMID19182773
PMCPMC2762424
OpenAlexW2051481258

What OpenQuestion holds

Textmetadata
LicenceTDM
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.