Evidence map›Paper›PMID 25312585›Full record

ArticleThe Journal of general virology2015

Glucocorticosteroids trigger reactivation of human cytomegalovirus from latently infected myeloid cells and increase the risk for HCMV infection in D+R+ liver transplant patients.

Ellen Van Damme, Sarah Sauviller, Betty Lau, Bart Kesteleyn, Paul Griffiths, Andrew Burroughs, Vincent Emery, John Sinclair, Marnix Van Loock

Open access · hybridAbstract read
In one paragraph

Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Guideline
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  4. Global cis-regulatory landscape of double-stranded DNA viruses.bioRxiv : the preprint server for biology · 2025
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  12. Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

9 authors at 5 institutions in 2 countries.

Ellen Van DammeJanssen Infectious Diseases BVBA, Turnhoutseweg 30, 2340 Beerse, Belgium.
Sarah SauvillerJanssen Infectious Diseases BVBA, Turnhoutseweg 30, 2340 Beerse, Belgium.
Betty LauDepartment of Medicine, University of Cambridge, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Bart KesteleynJanssen Infectious Diseases BVBA, Turnhoutseweg 30, 2340 Beerse, Belgium.
Paul GriffithsDivision of Infection and Immunity (Royal Free Campus), University College London, Rowland Hill Street, Hampstead, London NW3 2QG, UK.
Andrew BurroughsSheila Sherlock Liver Centre, Royal Free NHS Trust, Hampstead, London NW3 2QG, UK.
Vincent EmeryDepartment of Microbial and Cellular Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK.
John SinclairDepartment of Medicine, University of Cambridge, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Marnix Van LoockJanssen Infectious Diseases BVBA, Turnhoutseweg 30, 2340 Beerse, Belgium.
Janssen (Belgium) · BEAddenbrooke's Hospital · GBRoland Hill (United Kingdom) · GBRoyal Free London NHS Foundation Trust · GBThe Royal Free Hospital · GB

Funding

Medical Research Council G:0701279Medical Research Council G0701279Medical Research Council MR/K021087/1Wellcome Trust 078332
6 · The paper itself

Abstract

Graft rejection in transplant patients is managed clinically by suppressing T-cell function with immunosuppressive drugs such as prednisolone and methylprednisolone. In such immunocompromised hosts, human cytomegalovirus (HCMV) is an important opportunistic pathogen and can cause severe morbidity and mortality. Currently, the effect of glucocorticosteroids (GCSs) on the HCMV life cycle remains unclear. Previous reports showed enhanced lytic replication of HCMV in vitro in the presence of GCSs. In the present study, we explored the implications of steroid exposure on latency and reactivation. We observed a direct effect of several GCSs used in the clinic on the activation of a quiescent viral major immediate-early promoter in stably transfected THP-1 monocytic cells. This activation was prevented by the glucocorticoid receptor (GR) antagonist Ru486 and by shRNA-mediated knockdown of the GR. Consistent with this observation, prednisolone treatment of latently infected primary monocytes resulted in HCMV reactivation. Analysis of the phenotype of these cells showed that treatment with GCSs was correlated with differentiation to an anti-inflammatory macrophage-like cell type. On the basis that these observations may be pertinent to HCMV reactivation in post-transplant settings, we retrospectively evaluated the incidence, viral kinetics and viral load of HCMV in liver transplant patients in the presence or absence of GCS treatment. We observed that combination therapy of baseline prednisolone and augmented methylprednisolone, upon organ rejection, significantly increased the incidence of HCMV infection in the intermediate risk group where donor and recipient are both HCMV seropositive (D+R+) to levels comparable with the high risk D+R- group.

Indexed as

AdultAgedAged, 80 and overCell DifferentiationCell LineCommunicable DiseasesCytomegalovirusCytomegalovirus InfectionsFemaleGlucocorticoidsHumansImmunocompromised HostLiverLiver TransplantationMaleMiddle AgedGlucocorticoidsReceptors, Glucocorticoid

Identifiers

PMID25312585
PMCPMC4268819
OpenAlexW2058092457

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.