Evidence map›Paper›PMID 34290252›Full record

ArticleNature communications2021

Targeting the latent human cytomegalovirus reservoir for T-cell-mediated killing with virus-specific nanobodies.

Timo W M De Groof, Elizabeth G Elder, Eleanor Y Lim, Raimond Heukers, Nick D Bergkamp, Ian J Groves, Mark Wills, John H Sinclair, Martine J Smit

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  11. Nanobodies: Robust miniprotein binders in biomedicine.Advanced drug delivery reviews · 2023
    Review
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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 4 countries.

Timo W M De Groof *Amsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, VU University, De Boelelaan 1108, Amsterdam, The Netherlands.ORCID 0000-0001-6918-2955
Elizabeth G Elder *Department of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0003-1615-2642
Eleanor Y LimDepartment of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.
Raimond HeukersAmsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, VU University, De Boelelaan 1108, Amsterdam, The Netherlands.ORCID 0000-0003-4498-7751
Nick D BergkampAmsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, VU University, De Boelelaan 1108, Amsterdam, The Netherlands.
Ian J GrovesDepartment of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0001-8882-6701
Mark WillsDepartment of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.
John H SinclairDepartment of Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.
Martine J SmitAmsterdam Institute for Molecular and Life Sciences (AIMMS), Division of Medicinal Chemistry, Faculty of Science, VU University, De Boelelaan 1108, Amsterdam, The Netherlands. mj.smit@vu.nl.ORCID 0000-0003-2713-0238
University of Cambridge · GBVrije Universiteit Amsterdam · NLPublic Health Agency of Sweden · SEUniversity of Applied Sciences Utrecht · NLVrije Universiteit Brussel · BE

Funding

Department of HealthMedical Research Council MR/K021087/1Medical Research Council MR/S00081X/1Wellcome TrustWellcome Trust 109075/Z/15/A
6 · The paper itself

Abstract

Latent human cytomegalovirus (HCMV) infection is characterized by limited gene expression, making latent HCMV infections refractory to current treatments targeting viral replication. However, reactivation of latent HCMV in immunosuppressed solid organ and stem cell transplant patients often results in morbidity. Here, we report the killing of latently infected cells via a virus-specific nanobody (VUN100bv) that partially inhibits signaling of the viral receptor US28. VUN100bv reactivates immediate early gene expression in latently infected cells without inducing virus production. This allows recognition and killing of latently infected monocytes by autologous cytotoxic T lymphocytes from HCMV-seropositive individuals, which could serve as a therapy to reduce the HCMV latent reservoir of transplant patients.

Indexed as

Cells, CulturedCytomegalovirusCytomegalovirus InfectionsGene ExpressionGenes, Immediate-EarlyHumansLipopolysaccharide ReceptorsMonocytesReceptors, ChemokineSignal TransductionSingle-Domain AntibodiesT-Lymphocytes, CytotoxicViral ProteinsVirus ActivationVirus LatencyCD14 protein, humanLipopolysaccharide ReceptorsReceptors, ChemokineSingle-Domain AntibodiesUS28 receptor, CytomegalovirusViral Proteins

Identifiers

PMID34290252
PMCPMC8295288
OpenAlexW3184687174

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.