Evidence map›Paper›PMID 31569051›Full record

ArticleiScience2019

Human Cytomegalovirus Upregulates Expression of HCLS1 Resulting in Increased Cell Motility and Transendothelial Migration during Latency.

Yusuf Aslam, James Williamson, Veronika Romashova, Elizabeth Elder, Benjamin Krishna, Mark Wills, Paul Lehner, John Sinclair, Emma Poole

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Cytomegalovirus disrupts Lamin A/C to control microtubule-mediated nuclear movement and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  6. Frontiers in immunology · 2023
    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

9 authors at 3 institutions in 2 countries.

Yusuf AslamCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
James WilliamsonCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Veronika RomashovaCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Elizabeth ElderCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Benjamin KrishnaLerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA.
Mark WillsCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
Paul LehnerCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.
John SinclairCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK. Electronic address: js152@cam.ac.uk.
Emma PooleCambridge University, Department of Medicine, Level 5, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK. Electronic address: elp27@cam.ac.uk.
University of Cambridge · GBAddenbrooke's Hospital · GBCleveland Clinic Lerner College of Medicine · US

Funding

Medical Research Council G0701279Medical Research Council MR/K021087/1Medical Research Council MR/S00081X/1Wellcome Trust 210688/Z/18/Z
6 · The paper itself

Abstract

Human cytomegalovirus establishes a lifelong, latent infection in the human host and can cause significant morbidity and mortality, particularly, in immunocompromised individuals. One established site of HCMV latency and reactivation is in cells of the myeloid lineage. In undifferentiated myeloid cells, such as CD14+ monocytes, virus is maintained latently. We have recently reported an analysis of the total proteome of latently infected CD14+ monocytes, which identified an increase in hematopoietic lineage cell-specific protein (HCLS1). Here we show that this latency-associated upregulation of HCLS1 occurs in a US28-dependent manner and stabilizes actin structure in latently infected cells. This results in their increased motility and ability to transit endothelial cell layers. Thus, latency-associated increases in monocyte motility could aid dissemination of the latently infected reservoir, and targeting this increased motility could have an impact on the ability of latently infected monocytes to distribute to tissue sites of reactivation.

Indexed as

Cellular PhysiologyImmunologyVirology

Identifiers

PMID31569051
PMCPMC6817630
OpenAlexW2973067740

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.