Evidence map›Paper›PMID 27387220›Full record

ArticlePLoS pathogens2016

A Homolog Pentameric Complex Dictates Viral Epithelial Tropism, Pathogenicity and Congenital Infection Rate in Guinea Pig Cytomegalovirus.

Stewart Coleman, K Yeon Choi, Matthew Root, Alistair McGregor

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. A vaccine against cytomegalovirus: how close are we?The Journal of clinical investigation · 2025
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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

4 authors at 1 institution in 1 country.

Stewart ColemanDepartment of Microbial Pathogenesis & Immunology, Texas A&M University, Health Science Center, College of Medicine, College Station, Texas, United States of America.
K Yeon ChoiDepartment of Microbial Pathogenesis & Immunology, Texas A&M University, Health Science Center, College of Medicine, College Station, Texas, United States of America.
Matthew RootDepartment of Microbial Pathogenesis & Immunology, Texas A&M University, Health Science Center, College of Medicine, College Station, Texas, United States of America.ORCID 0000-0002-7667-4664
Alistair McGregorDepartment of Microbial Pathogenesis & Immunology, Texas A&M University, Health Science Center, College of Medicine, College Station, Texas, United States of America.
Texas A&M Health Science Center · US

Funding

Placental trophoblast infection and TLR mediated response to congenital CMVR01AI100933 · NIAID · UNIVERSITY OF MINNESOTA · PI MCGREGOR, ALISTAIR · 2012 to 2015
$1.5M
Development of an effective DISC vaccine strategy against congenital CMVR01AI098984 · NIAID · UNIVERSITY OF MINNESOTA · PI MCGREGOR, ALISTAIR · 2012 to 2015
$1.4M
Vaccine against CMV endothelial tropism & congenital infectionR21AI090156 · NIAID · UNIVERSITY OF MINNESOTA · PI MCGREGOR, ALISTAIR · 2012 to 2013
$389k
NIAID NIH HHS R01 AI098984NIAID NIH HHS R01 AI100933NIAID NIH HHS R21 AI090156
6 · The paper itself

Abstract

In human cytomegalovirus (HCMV), tropism to epithelial and endothelial cells is dependent upon a pentameric complex (PC). Given the structure of the placenta, the PC is potentially an important neutralizing antibody target antigen against congenital infection. The guinea pig is the only small animal model for congenital CMV. Guinea pig cytomegalovirus (GPCMV) potentially encodes a UL128-131 HCMV PC homolog locus (GP128-GP133). In transient expression studies, GPCMV gH and gL glycoproteins interacted with UL128, UL130 and UL131 homolog proteins (designated GP129 and GP131 and GP133 respectively) to form PC or subcomplexes which were determined by immunoprecipitation reactions directed to gH or gL. A natural GP129 C-terminal deletion mutant (aa 107-179) and a chimeric HCMV UL128 C-terminal domain swap GP129 mutant failed to form PC with other components. GPCMV infection of a newly established guinea pig epithelial cell line required a complete PC and a GP129 mutant virus lacked epithelial tropism and was attenuated in the guinea pig for pathogenicity and had a low congenital transmission rate. Individual knockout of GP131 or 133 genes resulted in loss of viral epithelial tropism. A GP128 mutant virus retained epithelial tropism and GP128 was determined not to be a PC component. A series of GPCMV mutants demonstrated that gO was not strictly essential for epithelial infection whereas gB and the PC were essential. Ectopic expression of a GP129 cDNA in a GP129 mutant virus restored epithelial tropism, pathogenicity and congenital infection. Overall, GPCMV forms a PC similar to HCMV which enables evaluation of PC based vaccine strategies in the guinea pig model.

Indexed as

Disease Models, AnimalHerpesviridaeAnimalsCytomegalovirusCytomegalovirus InfectionsEpithelial CellsFemaleGene Knockout TechniquesGuinea PigsHerpesviridae InfectionsImmunoprecipitationMembrane GlycoproteinsMutagenesis, Site-DirectedPlacentaPregnancyPregnancy Complications, InfectiousMembrane GlycoproteinsViral Envelope Proteins

Identifiers

PMID27387220
PMCPMC4936736
OpenAlexW2471390345

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.