Evidence map›Paper›PMID 12719548›Full record

ArticleJournal of virology2003

Role of murine cytomegalovirus US22 gene family members in replication in macrophages.

Carine Ménard, Markus Wagner, Zsolt Ruzsics, Karina Holak, Wolfram Brune, Ann E Campbell, Ulrich H Koszinowski

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 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

106 citing papers in PubMed, 175 citations in OpenAlex.

  1. Review
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  10. Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023
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  11. Antagonism of Protein Kinase R by Large DNA Viruses.Pathogens (Basel, Switzerland) · 2022
    Review
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  15. Article
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  18. Article
  19. Cytomegalovirus inhibition of extrinsic apoptosis determines fitness and resistance to cytotoxic CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  20. Article

46 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

7 authors at 2 institutions in 2 countries.

Carine MénardDepartment of Virology, Max von Pettenkofer Institute, Ludwig Maximilians University Munich, 80336 Munich, Germany.
Markus Wagner
Zsolt Ruzsics
Karina Holak
Wolfram Brune
Ann E Campbell
Ulrich H Koszinowski
Ludwig-Maximilians-Universität München · DEEastern Virginia Medical School · US

Funding

GENETIC DETERMINANTS OF CYTOMEGALOVIRUS PATHOGENESISR01CA041451 · NCI · EASTERN VIRGINIA MEDICAL SCHOOL · PI CAMPBELL, ANN E · 1992 to 2007
$1.7M
NCI NIH HHS R01 CA041451
6 · The paper itself

Abstract

The large cytomegalovirus (CMV) US22 gene family, found in all betaherpesviruses, comprises 12 members in both human cytomegalovirus (HCMV) and murine cytomegalovirus (MCMV). Conserved sequence motifs suggested a common ancestry and related functions for these gene products. Two members of this family, m140 and m141, were recently shown to affect MCMV replication on macrophages. To test the role of all US22 members in cell tropism, we analyzed the growth properties in different cell types of MCMV mutants carrying transposon insertions in all 12 US22 gene family members. When necessary, additional targeted mutants with gene deletions, ATG deletions, and ectopic gene revertants were constructed. Mutants with disruption of genes M23, M24, m25.1, m25.2, and m128 (ie2) showed no obvious growth phenotype, whereas growth of M43 mutants was reduced in a number of cell lines. Genes m142 and m143 were shown to be essential for virus replication. Growth of mutants with insertions into genes M36, m139, m140, and m141 in macrophages was severely affected. The common phenotype of the m139, m140, and m141 mutants was explained by an interaction at the protein level. The M36-dependent macrophage growth phenotype could be explained by the antiapoptotic function of the gene that was required for growth on macrophages but not for growth on other cell types. Together, the comprehensive set of mutants of the US22 gene family suggests that individual family members have diverged through evolution to serve a variety of functions for the virus.

Indexed as

Virus Replication3T3 CellsAnimalsApoptosisCell LineCells, CulturedDNA Transposable ElementsGene Expression Regulation, ViralHerpesviridae InfectionsImmediate-Early ProteinsMacrophagesMacrophages, PeritonealMiceMice, Inbred BALB CMuromegalovirusMutagenesis, InsertionalDNA Transposable ElementsImmediate-Early Proteins

Identifiers

PMID12719548
PMCPMC154053
OpenAlexW2132025920

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.