Evidence map›Paper›PMID 12140743›Full record

ReviewGenes and immunity2002

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match.

J R Webb, S H Lee, S M Vidal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Genes and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Methods for Studying the Function of Cytomegalovirus GPCRs.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Analysis of the MCMV resistome by ENU mutagenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2006
    Article
  15. Immunization with hepatitis C virus-like particles protects mice from recombinant hepatitis C virus-vaccinia infection.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  16. Looking back and looking forward.Genes and immunity · 2003
    Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

J R WebbDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ontario, K1H 8M5, Canada.
S H Lee
S M Vidal
University of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytomegalovirus (CMV) is a widespread pathogen that is responsible for severe disease in immunocompromised individuals and probably, associated with vascular disease in the general population. There is increasing evidence that cells of the innate immune system play a key role in controlling this important pathogen. This is particularly evident in the experimental murine CMV (MCMV) model of infection which has revealed an important role for natural killer (NK) cells in controlling early viral replication after infection with MCMV. In this model, different strains of inbred mice exhibit striking differences in their level of susceptibility to MCMV infection. Genetic studies, performed almost 10 years ago, revealed that this pattern of susceptibility/resistance can be attributed to a single genetic locus termed Cmv1 and recently several groups that have been working on the mapping and identification of Cmv1 have met with success. Interestingly, Cmv1 is allelic to a member of the Ly49 gene family, which encode activating or inhibitory transmembrane receptors present on the surface of NK cells. All Ly49 receptors characterized to date interact with MHC class I molecules on potential target cells, resulting in the accumulation of signals to the NK to either 'kill' or 'ignore' the cell based upon the repertoire of MHC class I molecules expressed. The identification of Cmv1 as Ly49H, a stimulatory member of the Ly49 family, adds an interesting twist to the Ly49 story. Although the ligand of Ly49H is not yet known, there is already compelling evidence that the ligand is upregulated on virally infected cells, resulting in specific activation of Ly49H-expressing NK cells. This review provides an historical perspective of the MCMV infection model from its inception to the discovery of the gene responsible for the phenotype and provides a basis for further experiments aimed at understanding the role of NK cells, in general, and Ly49H, in particular, in mediating resistance to cytomegalovirus.

Indexed as

AnimalsAntigens, LyChromosome MappingCloning, MolecularCytomegalovirusCytomegalovirus InfectionsDisease Models, AnimalHumansImmunity, InnateKiller Cells, NaturalLectins, C-TypeMiceModels, ImmunologicalNK Cell Lectin-Like Receptor Subfamily AReceptors, NK Cell Lectin-LikeVirus ReplicationAntigens, LyKlra8 protein, mouseLectins, C-TypeNK Cell Lectin-Like Receptor Subfamily AReceptors, NK Cell Lectin-Like

Identifiers

PMID12140743
OpenAlexW2025063123

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.