Evidence map›Paper›PMID 21852192›Full record

ArticleTrends in molecular medicine2011

All is fair in virus-host interactions: NK cells and cytomegalovirus.

Marina Babić, Astrid Krmpotić, Stipan Jonjić

Open access · greenAbstract read
In one paragraph

Article in Trends in molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Tuning the Orchestra: HCMV vs. Innate Immunity.Frontiers in microbiology · 2020
    Review
  7. Review
  8. Article
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  14. Review
  15. Article
  16. Modulation of CD112 by the alphaherpesvirus gD protein suppresses DNAM-1-dependent NK cell-mediated lysis of infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. Article
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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 1 institution in 1 country.

Marina BabićDepartment of Histology and Embryology, Faculty of Medicine, University of Rijeka, B. Branchetta 20, 51 000 Rijeka, Croatia.
Astrid Krmpotić
Stipan Jonjić
University of Rijeka · HR

Funding

Viral evasion of NK cellsR01AI083201 · NIAID · UNIVERSITY OF RIJEKA--MEDICAL FACULTY · PI JONJIC, STIPAN · 2009 to 2012
$331k
NIAID NIH HHS 1R01AI083201-01NIAID NIH HHS R01 AI083201
6 · The paper itself

Abstract

The infection of mice with mouse cytomegalovirus (MCMV) as a model of human cytomegalovirus (HCMV) infection has been particularly informative in elucidating the role of innate and adaptive immune response mechanisms during infection. Millions of years of co-evolution between cytomegaloviruses (CMV) and their hosts has resulted in numerous attempts to overwhelm each other. CMVs devote many genes to modulating the host natural killer (NK) cell response and NK cells employ many strategies to cope with CMV infection. While focusing on these attack-counterattack measures, this review will discuss several novel mechanisms of immune evasion by MCMV, the role of Ly49 receptors in mediating resistance to MCMV, and the impact of the initial NK cell response on the shaping of adaptive immunity.

Indexed as

Immune EvasionAdaptive ImmunityAnimalsCytomegalovirusCytomegalovirus InfectionsDisease Models, AnimalHumansKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily ANK Cell Lectin-Like Receptor Subfamily KKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily ANK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID21852192
PMCPMC3205326
OpenAlexW2095498551

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.