Evidence map›Paper›PMID 39205246›Full record

ReviewViruses2024

No Time to Die: How Cytomegaloviruses Suppress Apoptosis, Necroptosis, and Pyroptosis.

Yingqi Deng, Ana Águeda-Pinto, Wolfram Brune

Abstract readReview
In one paragraph

Review in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. 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.

Yingqi DengLeibniz Institute of Virology (LIV), 20251 Hamburg, Germany.ORCID 0000-0001-6403-3096
Ana Águeda-PintoLeibniz Institute of Virology (LIV), 20251 Hamburg, Germany.
Wolfram BruneLeibniz Institute of Virology (LIV), 20251 Hamburg, Germany.ORCID 0000-0002-6078-5255

Funding

China Scholarship Council 201706170063Landesforschungsförderung LFF LV74
6 · The paper itself

Abstract

Viruses are obligate intracellular pathogens as their replication depends on the metabolism of the host cell. The induction of cellular suicide, known as programmed cell death (PCD), has the potential to hinder viral replication and act as a first line of defense against viral pathogens. Apoptosis, necroptosis, and pyroptosis are three important PCD modalities. Different signaling pathways are involved in their execution, and they also differ in their ability to cause inflammation. Cytomegaloviruses (CMV), beta-herpesviruses with large double-stranded DNA genomes, encode a great variety of immune evasion genes, including several cell death suppressors. While CMV inhibitors of apoptosis and necroptosis have been known and studied for years, the first pyroptosis inhibitor has been identified and characterized only recently. Here, we describe how human and murine CMV interfere with apoptosis, necroptosis, and pyroptosis signaling pathways. We also discuss the importance of the different PCD forms and their viral inhibitors for the containment of viral replication and spread in vivo.

Indexed as

ApoptosisCytomegalovirusNecroptosisPyroptosisSignal TransductionVirus ReplicationAnimalsCytomegalovirus InfectionsHost-Pathogen InteractionsHumansImmune EvasionMiceapoptosiscell deathcytomegalovirusimmune evasionnecroptosispyroptosis

Identifiers

PMID39205246
PMCPMC11359067

What OpenQuestion holds

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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.