Evidence map›Paper›PMID 12584345›Full record

ArticleJournal of virology2003

An essential role of the enhancer for murine cytomegalovirus in vivo growth and pathogenesis.

Peter Ghazal, Martin Messerle, Kent Osborn, Ana Angulo

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. 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
2.2field-weighted citation impact, top 12% 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, 35 citations in OpenAlex.

  1. Methods for Studying the Function of Cytomegalovirus GPCRs.Methods in molecular biology (Clifton, N.J.) · 2021
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  7. Murine cytomegalovirus IE3 protein interacts with Ankrd17.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011
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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 2 institutions in 2 countries.

Peter GhazalDepartment of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
Martin Messerle
Kent Osborn
Ana Angulo
Scripps Research Institute · USInstitute of Medical Microbiology and Hygiene · DE

Funding

EVOLVING SYNTHETIC POLYAMIDES AGAINST CYTOMEGALOVIRUSR21AI044851 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI ANGULO, ANA · 2000 to 2000
$266k
TRANSCRIPTION FACTORS AND HUMAN CMV PATHOGENESISR01AI030627 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI GHAZAL, PETER · 1997 to 1999
–
TRANSCRIPTION FACTORS AND HUMAN CMV PATHOGENESISR29AI030627 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI GHAZAL, PETER · 1992 to 1996
–
NIAID NIH HHS AI-30627NIAID NIH HHS AI-44851
6 · The paper itself

Abstract

The transcription of cytomegalovirus (CMV) immediate-early (IE) genes is regulated by a large and complex enhancer containing an array of binding sites for a variety of cellular transcription factors. Previously, using bacterial artificial chromosome recombinants of the virus genome, it was reported that the enhancer region of murine CMV (MCMV) is dispensable but performs a key function for viral multiplication (A. Angulo, M. Messerle, U. H. Koszinowski, and P. Ghazal, J. Virol. 72:8502-8509, 1998). In the present study, we defined, through the reconstitution of infectious enhancerless MCMVs, the growth requirement for the enhancer in tissue culture and explored its significance for steering a productive infection in vivo. A comparison of cis and trans complementation systems for infection of enhancerless virus in permissive fibroblasts revealed a multiplicity-dependent growth phenotype that is severely compromised in the rate of infectious-virus multiplication. The in vivo impact of viruses that have an amputated enhancer was investigated in an extremely sensitive model of MCMV infection, the SCID mouse. Histological examination of spleens, livers, lungs, and salivary glands from animals infected with enhancer-deficient MCMV demonstrated an absence of tissue damage associated with CMV infection. The lack of pathogenic lesions correlated with a defect in replication competence. Enhancerless viruses were not detectable in major target organs harvested from SCID mice. The pathogenesis and growth defect reverted upon restoration of the enhancer. Markedly, while SCID mice infected with 5 PFU of parental MCMV died within 50 days postinfection, all mice infected with enhancerless virus survived for the duration of the experiment (1 year) after infection with 5 x 10(5) PFU. Together, these results clarify the importance of the enhancer for MCMV growth in cell culture and underscore the in vivo significance of this region for MCMV virulence and pathogenesis.

Indexed as

3T3 CellsAnimalsCell LineChromosomes, Artificial, BacterialEnhancer Elements, GeneticFemaleGene Expression Regulation, ViralHerpesviridae InfectionsImmediate-Early ProteinsMiceMice, SCIDMuromegalovirusMutationPromoter Regions, GeneticTranscription, GeneticVirulenceImmediate-Early Proteins

Identifiers

PMID12584345
PMCPMC149741
OpenAlexW2040640331

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.