Evidence map›Paper›PMID 31375588›Full record

ArticleJournal of virology2019

Establishment of a Virulent Full-Length cDNA Clone for Type I Feline Coronavirus Strain C3663.

Yutaka Terada, Yudai Kuroda, Shigeru Morikawa, Yoshiharu Matsuura, Ken Maeda, Wataru Kamitani

Abstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Systematizing the genomic order and relatedness in the open reading frames (ORFs) of the coronaviruses.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2021
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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

6 authors at 3 institutions in 1 country.

Yutaka TeradaLaboratory of Clinical Research on Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yudai KurodaLaboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan.
Shigeru MorikawaDepartment of Veterinary Science, National Institute of Infectious Diseases, Tokyo, Japan.ORCID 0000-0001-6249-6716
Yoshiharu MatsuuraDepartment of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Ken MaedaLaboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan.
Wataru KamitaniLaboratory of Clinical Research on Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan wakamita@biken.osaka-u.ac.jp.
Yamaguchi University · JPThe University of Osaka · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Feline infectious peritonitis (FIP) is one of the most important infectious diseases in cats and is caused by feline coronavirus (FCoV). Tissue culture-adapted type I FCoV shows reduced FIP induction in experimental infections, which complicates the understanding of FIP pathogenesis caused by type I FCoV. We previously found that the type I FCoV strain C3663 efficiently induces FIP in specific-pathogen-free cats through the naturally infectious route. In this study, we employed a bacterial artificial chromosome-based reverse genetics system to gain more insights into FIP caused by the C3633 strain. We successfully generated recombinant virus (rC3663) from Fcwf-4 cells transfected with infectious cDNA that showed growth kinetics similar to those shown by the parental virus. Next, we constructed a reporter C3663 virus carrying the nanoluciferase (Nluc) gene to measure viral replication with high sensitivity. The inhibitory effects of different compounds against rC3663-Nluc could be measured within 24 h postinfection. Furthermore, we found that A72 cells derived from canine fibroblasts permitted FCoV replication without apparent cytopathic effects. Thus, our reporter virus is useful for uncovering the infectivity of type I FCoV in different cell lines, including canine-derived cells. Surprisingly, we uncovered aberrant viral RNA transcription of rC3663 in A72 cells. Overall, we succeeded in obtaining infectious cDNA clones derived from type I FCoV that retained its virulence. Our recombinant FCoVs are powerful tools for increasing our understanding of the viral life cycle and pathogenesis of FIP-inducing type I FCoV.

Indexed as

Virus ReplicationAnimalsCatsCoronavirus, FelineCoronavirus InfectionsDNA, ComplementaryDogsFeline Infectious PeritonitisGenome, ViralMadin Darby Canine Kidney CellsRNA, ViralVirulenceDNA, ComplementaryRNA, Viralcoronavirusviral replication

Identifiers

PMID31375588
PMCPMC6803248
OpenAlexW2966849695

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.