Evidence map›Paper›PMID 15331722›Full record

ArticleJournal of virology2004

Molecular, biological, and in vivo characterization of the guinea pig cytomegalovirus (CMV) homologs of the human CMV matrix proteins pp71 (UL82) and pp65 (UL83).

Alistair McGregor, Fenyong Liu, Mark R Schleiss

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

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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

3 authors at 3 institutions in 1 country.

Alistair McGregorDivision of Infectious Diseases, Children's Hospital Medical Center Research Foundation, University of Cincinnati, OH 45229, USA.
Fenyong Liu
Mark R Schleiss
Children's Hospital Foundation · USUniversity of California, Berkeley · USUniversity of Cincinnati · US

Funding

Viral Immunomodulation and Rational CMV Vaccine DesignR01HD044864 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI GEBALLE, ADAM P., MCVOY, MICHAEL A · 2003 to 2015
$4.5M
VACCINES FOR PREVENTION OF EXPERIMENTAL CONGENITAL CMVR01HD038416 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI SCHLEISS, MARK R. · 2000 to 2009
$2.2M
Novel Immunostimulant/Adjuvant for HIV Vaccines: Non-Human Primate StudiesR43AI065289 · NIAID · JUVARIS BIOTHERAPEUTICS, INC. · PI WARNER, JOHN F · 2006 to 2007
$537k
NIAID NIH HHS AI65289NIAID NIH HHS R43 AI065289NICHD NIH HHS HD38416-01NICHD NIH HHS HD44864-01NICHD NIH HHS R01 HD038416NICHD NIH HHS R01 HD044864
6 · The paper itself

Abstract

We recently identified the genes encoding the guinea pig cytomegalovirus (GPCMV) homologs of the upper and lower matrix proteins of human CMV, pp71 (UL82) and pp65 (UL83), which we designated GP82 and GP83, respectively. Transient-expression studies with a GP82 plasmid demonstrated that the encoded protein targets the nucleus and that the infectivity and plaquing efficiency of cotransfected GPCMV viral DNA was enhanced by GP82. The transactivation function of GP82 was not limited to GPCMV, but was also observed for a heterologous virus, herpes simplex virus type 1 (HSV-1). This was confirmed by its ability to complement the growth of an HSV-1 VP16 transactivation-defective mutant virus in an HSV viral DNA cotransfection assay. Study of a GP82 "knockout" virus (and its attendant rescuant), generated on a GPCMV bacterial artificial chromosome construct, confirmed the essential nature of the gene. Conventional homologous recombination was used to generate a GP83 mutant to examine the role of GP83 in the viral life cycle. Comparison of the one-step growth kinetics of the GP83 mutant (vAM409) and wild-type GPCMV indicated that GP83 protein is not required for viral replication in tissue culture. The role of GP83 in vivo was examined by comparing the pathogenesis of wild-type GPCMV, vAM409, and a control virus, vAM403, in guinea pigs. The vAM409 mutant was significantly attenuated for dissemination in immunocompromised strain 2 guinea pigs, suggesting that the GP83 protein is essential for full pathogenicity in vivo.

Indexed as

Amino Acid SequenceAnimalsBase SequenceCell LineChromosomes, Artificial, BacterialCloning, MolecularCytomegalovirusDNA, ViralGenes, ViralGuinea PigsHumansMolecular Sequence DataMutagenesisOpen Reading FramesPhosphoproteinsRoseoloviruscytomegalovirus matrix protein 65kDacytomegalovirus phosphoprotein 71kDaDNA, ViralPhosphoproteinsViral Matrix ProteinsViral Proteins

Identifiers

PMID15331722
PMCPMC515002
OpenAlexW2120154091

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.