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Richard J. Stanton

Researcher at Cardiff University

Publications -  92
Citations -  3557

Richard J. Stanton is an academic researcher from Cardiff University. The author has contributed to research in topics: Human cytomegalovirus & Virus. The author has an hindex of 27, co-authored 70 publications receiving 2865 citations. Previous affiliations of Richard J. Stanton include University Hospital of Wales & University of Cambridge.

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Quantitative temporal viromics: an approach to investigate host-pathogen interaction.

TL;DR: A systematic quantitative analysis of temporal changes in host and viral proteins throughout the course of a productive infection could provide dynamic insights into virus-host interaction, applicable to any virus with a robust in vitro model.
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Modulation of natural killer cells by human cytomegalovirus

TL;DR: The mechanisms by which HCMV systematically evades (or, more properly, modulates) NK cell recognition constitutes an area of growing understanding that is enhancing the authors' appreciation of the basic mechanisms of NK cell function in humans.
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Reconstruction of the complete human cytomegalovirus genome in a BAC reveals RL13 to be a potent inhibitor of replication

TL;DR: To overcome rapid emergence of mutations in genetically intact HCMV, a system in which RL13 and UL131A were conditionally repressed during virus propagation is developed, which permits studies to be undertaken with a clonal, characterized H CMV strain containing the complete wild-type gene complement.
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Sequential mutations associated with adaptation of human cytomegalovirus to growth in cell culture

TL;DR: Results suggest strongly that RL13 and UL128L exert at least partially independent suppressive effects on growth in fibroblasts, particularly those involved in cell tropism, immune evasion or growth temperance.
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The human cytomegalovirus MHC class I homolog UL18 inhibits LIR-1+ but activates LIR-1- NK cells.

TL;DR: In this study, LIR-1+ NKL cell-mediated cytotoxicity was shown to be inhibited by transduction of targets with a replication-deficient adenovirus vector encoding UL18 (RAd-UL18) and fibroblasts infected with an HCMV UL18 mutant also exhibited enhanced susceptibility to NKL killing relative to cells infected with the parental virus.