Evidence map›Paper›PMID 39298313›Full record

ArticleCell reports2024

Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms.

Alejandro Casco, Makoto Ohashi, Eric Johannsen

Abstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  6. 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

3 authors.

Alejandro CascoDepartment of Oncology, McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA.
Makoto OhashiDepartment of Oncology, McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA.
Eric JohannsenDepartment of Oncology, McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI, USA; Department of Medicine, Division of Infectious Diseases, University of Wisconsin, Madison, WI, USA. Electronic address: ejohannsen@medicine.wisc.edu.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Paul F. Lambert · 1985 to 2026
$53.1M
Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Role of Epstein-Barr virus LMP2A protein in maintaining oncogenic IgM signaling in EBV+ B cell lymphomasU01CA275247 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI ERIC C JOHANNSEN · 2022 to 2026
$2.2M
NCI NIH HHS P01 CA022443NCI NIH HHS P30 CA014520NCI NIH HHS T32 CA009135NCI NIH HHS U01 CA275247
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is a ubiquitous oncogenic virus associated with multiple cancers and autoimmune diseases. Unlike most herpesviruses, EBV reactivation from latency occurs asymptomatically, allowing it to spread efficiently to other hosts. However, available models are limited by the inefficient and asynchronous reactivation from latency into lytic replication. To address this problem, we develop a dual-fluorescent lytic reporter (DFLR) EBV that specifically labels cells in the early and late stages of replication. Using lymphoblastoid cell lines transformed by DFLR EBV as a model for EBV reactivation in B cells, we observe extensive reprogramming of the host cell transcriptome during lytic cycle progression. This includes widespread shutoff of host gene expression and disruption of mRNA processing. Unexpectedly, host shutoff remains extensive even in cells infected with DFLR EBV deleted for the BGLF5 nuclease. These findings implicate BGLF5-independent mechanisms as the primary drivers of host transcriptome remodeling during EBV lytic replication.

Indexed as

Herpesvirus 4, HumanB-LymphocytesDeoxyribonucleasesEpstein-Barr Virus InfectionsHost-Pathogen InteractionsHumansTranscriptomeViral ProteinsVirus ActivationVirus LatencyVirus Replicationdeoxyribonuclease, Epstein-Barr virusDeoxyribonucleasesViral ProteinsCP: ImmunologyCP: MicrobiologyEBVherpesvirushost shutofflytic reactivationsplicingtranscriptomicstumor virus

Identifiers

PMID39298313
PMCPMC11549945

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.