Evidence map›Paper›PMID 12368349›Full record

ArticleJournal of virology2002

Systematic assembly of a full-length infectious cDNA of mouse hepatitis virus strain A59.

Boyd Yount, Mark R Denison, Susan R Weiss, Ralph S Baric

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed
21.7field-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

239 citing papers in PubMed, 329 citations in OpenAlex.

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179 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

4 authors at 3 institutions in 1 country.

Boyd YountDepartment of Epidemiology, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7435, USA.
Mark R Denison
Susan R Weiss
Ralph S Baric
University of North Carolina at Chapel Hill · USUniversity of Pennsylvania · USVanderbilt University Medical Center · US

Funding

POLYMERASE PROTEINS IN CORONAVIRUS REPLICATIONR01AI026603 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DENISON, MARK R · 1994 to 2014
$4.1M
STUDIES INTO THE MECHANISMS FOR MHV REPLICATIONR01AI023946 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 1986 to 2007
$2.3M
CORONAVIRUSES: MOLECULAR BIOLOGY AND PERSISTENCER01AI017418 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISS, SUSAN R. · 1985 to 2004
$1.4M
REVERSE GENETICS WITH A CORONAVIRUS INFECTIOUS CONSTRUCTR01GM063228 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 2001 to 2004
$1.0M
CORONAVIRUS--ANALYSIS OF POLYMERASE GENE PRODUCTSR29AI026603 · NIAID · VANDERBILT UNIVERSITY · PI DENISON, MARK R · 1988 to 1992
–
NIAID NIH HHS AI17418NIAID NIH HHS AI23946NIAID NIH HHS AI26603NIAID NIH HHS R01 AI017418NIAID NIH HHS R01 AI023946NIAID NIH HHS R01 AI026603NIGMS NIH HHS GM63228NIGMS NIH HHS R01 GM063228
6 · The paper itself

Abstract

A novel method was developed to assemble a full-length infectious cDNA of the group II coronavirus mouse hepatitis virus strain A59 (MHV-A59). Seven contiguous cDNA clones that spanned the 31.5-kb MHV genome were isolated. The ends of the cDNAs were engineered with unique junctions and assembled with only the adjacent cDNA subclones, resulting in an intact MHV-A59 cDNA construct of approximately 31.5 kb in length. The interconnecting restriction site junctions that are located at the ends of each cDNA are systematically removed during the assembly of the complete full-length cDNA product, allowing reassembly without the introduction of nucleotide changes. RNA transcripts derived from the full-length MHV-A59 construct were infectious, although transfection frequencies were enhanced 10- to 15-fold in the presence of transcripts encoding the nucleocapsid protein N. Plaque-purified virus derived from the infectious construct replicated efficiently and displayed similar growth kinetics, plaque morphology, and cytopathology in murine cells as did wild-type MHV-A59. Molecularly cloned viruses recognized the MHV receptor (MHVR) for docking and entry, and pretreatment of cells with monoclonal antibodies against MHVR blocked virus entry and replication. Cells infected with molecularly cloned MHV-A59 virus expressed replicase (gene 1) proteins identical to those of laboratory MHV-A59. Importantly, the molecularly cloned viruses contained three marker mutations that had been derived from the engineered component clones. Full-length infectious constructs of MHV-A59 will permit genetic modifications of the entire coronavirus genome, particularly in the replicase gene. The method has the potential to be used to construct viral, microbial, or eukaryotic genomes approaching several million base pairs in length and used to insert restriction sites at any given nucleotide in a microbial genome.

Indexed as

AnimalsCell LineCricetinaeDNA, ViralMiceMurine hepatitis virusPhenotypeRNA-Dependent RNA PolymeraseTumor Cells, CulturedViral ProteinsDNA, Viralgene 1 protein, CoronavirusRNA-Dependent RNA PolymeraseViral Proteins

Identifiers

PMID12368349
PMCPMC136593
OpenAlexW2131887043

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.