Evidence map›Paper›PMID 18334634›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Advantages of a single-cycle production assay to study cell culture-adaptive mutations of hepatitis C virus.

Rodney S Russell, Jean-Christophe Meunier, Shingo Takikawa, Kristina Faulk, Ronald E Engle, Jens Bukh, Robert H Purcell, Suzanne U Emerson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 168 citations in OpenAlex.

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  13. miR-122-based therapies select for three distinct resistance mechanisms based on alterations in RNA structure.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  15. Hepatitis C virus modulates signal peptide peptidase to alter host protein processing.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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50 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Rodney S RussellHepatitis Viruses and Molecular Hepatitis Sections, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Jean-Christophe Meunier
Shingo Takikawa
Kristina Faulk
Ronald E Engle
Jens Bukh
Robert H Purcell
Suzanne U Emerson
Hepatitis B Foundation · USNational Institutes of Health · US

Funding

Pathogenesis of Parenteral Viral HepatitisZIAAI001015 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI PURCELL, ROBERT H. · 2009 to 2012
$3.0M
Pathogenesis of Parenteral Viral HepatitisZ01AI001015 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI PURCELL, ROBERT H. · 2007 to 2008
$1.2M
Molecular Studies of Hepatitis C Virus.Z01AI000970 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI EMERSON, SUZANNE U · 2006 to 2008
$749k
Molecular Studies of Hepatitis C Virus.ZIAAI000970 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI EMERSON, SUZANNE U · 2009 to 2011
$712k
Intramural NIH HHS
6 · The paper itself

Abstract

The JFH1 strain of hepatitis C virus (HCV) is unique among HCV isolates, in that the wild-type virus can traverse the entire replication cycle in cultured cells. However, without adaptive mutations, only low levels of infectious virus are produced. In the present study, the effects of five mutations that were selected during serial passage in Huh-7.5 cells were studied. Recombinant genomes containing all five mutations produced 3-4 logs more infectious virions than did wild type. Neither a coding mutation in NS5A nor a silent mutation in E2 was adaptive, whereas coding mutations in E2, p7, and NS2 all increased virus production. A single-cycle replication assay in CD81-deficient cells was developed to study more precisely the effect of the adaptive mutations. The E2 mutation had minimal effect on the amount of infectious virus released but probably enhanced entry into cells. In contrast, both the p7 and NS2 mutations independently increased the amount of virus released.

Indexed as

Adaptation, BiologicalCell Culture TechniquesCell Line, TumorHepacivirusHumansMutationVirus Replication

Identifiers

PMID18334634
PMCPMC2393785
OpenAlexW2131143399

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.