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Modulation of natural killer cells by human cytomegalovirus

Overview of attention for article published in Journal of Clinical Virology, March 2008
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (75th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

Mentioned by

patent
3 patents

Citations

dimensions_citation
198 Dimensions

Readers on

mendeley
166 Mendeley
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Title
Modulation of natural killer cells by human cytomegalovirus
Published in
Journal of Clinical Virology, March 2008
DOI 10.1016/j.jcv.2007.10.027
Pubmed ID
Authors

Gavin W.G. Wilkinson, Peter Tomasec, Richard J. Stanton, Melanie Armstrong, Virginie Prod’homme, Rebecca Aicheler, Brian P. McSharry, Carole R. Rickards, Daniel Cochrane, Sian Llewellyn-Lacey, Eddie C.Y. Wang, Cora A. Griffin, Andrew J. Davison

Abstract

Human cytomegalovirus (HCMV) causes lifelong, persistent infections and its survival is under intense, continuous selective pressure from the immune system. A key aspect of HCMV's capacity for survival lies in immune avoidance. In this context, cells undergoing productive infection exhibit remarkable resistance to natural killer (NK) cell-mediated cytolysis in vitro. To date, six genes encoding proteins (UL16, UL18, UL40, UL83, UL141 and UL142) and one encoding a microRNA (miR-UL112) have been identified as capable of suppressing NK cell recognition. Even though HCMV infection efficiently activates expression of ligands for the NK cell activating receptor NKG2D, at least three functions (UL16, UL142 and miR-UL112) act in concert to suppress presentation of these ligands on the cell surface. Although HCMV downregulates expression of endogenous MHC-I, it encodes an MHC-I homologue (UL18) and also upregulates the expression of cellular HLA-E through the action of UL40. The disruption of normal intercellular connections exposes ligands for NK cell activating receptors on the cell surface, notably CD155. HCMV overcomes this vulnerability by encoding a function (UL141) that acts post-translationally to suppress cell surface expression of CD155. The mechanisms by which HCMV systematically evades (or, more properly, modulates) NK cell recognition constitutes an area of growing understanding that is enhancing our appreciation of the basic mechanisms of NK cell function in humans.

Mendeley readers

The data shown below were compiled from readership statistics for 166 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 4 2%
Portugal 2 1%
Israel 1 <1%
France 1 <1%
Germany 1 <1%
Singapore 1 <1%
United States 1 <1%
Unknown 155 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 38 23%
Researcher 34 20%
Student > Master 22 13%
Student > Bachelor 22 13%
Professor > Associate Professor 7 4%
Other 26 16%
Unknown 17 10%
Readers by discipline Count As %
Agricultural and Biological Sciences 69 42%
Medicine and Dentistry 25 15%
Biochemistry, Genetics and Molecular Biology 21 13%
Immunology and Microbiology 20 12%
Chemical Engineering 2 1%
Other 8 5%
Unknown 21 13%

Attention Score in Context

This research output has an Altmetric Attention Score of 6. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 January 2020.
All research outputs
#3,489,132
of 17,367,552 outputs
Outputs from Journal of Clinical Virology
#304
of 1,800 outputs
Outputs of similar age
#66,503
of 270,967 outputs
Outputs of similar age from Journal of Clinical Virology
#8
of 44 outputs
Altmetric has tracked 17,367,552 research outputs across all sources so far. Compared to these this one has done well and is in the 76th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,800 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.9. This one has done well, scoring higher than 77% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 270,967 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 75% of its contemporaries.
We're also able to compare this research output to 44 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.