Evidence map›Paper›PMID 18495760›Full record

ArticleJournal of virology2008

Establishment of B-cell lines latently infected with reactivation-competent murine gammaherpesvirus 68 provides evidence for viral alteration of a DNA damage-signaling cascade.

J Craig Forrest, Samuel H Speck

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

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  6. Evaluation of immune sensor responses to a viral small noncoding RNA.Frontiers in cellular and infection microbiology · 2024
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  19. Genipin as a novel chemical activator of EBV lytic cycle.Journal of microbiology (Seoul, Korea) · 2015
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

J Craig ForrestThe Emory Vaccine Center and Department of Microbiology & Immunology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Samuel H Speck
Emory University · US

Funding

Role of B Cells in Murine Gammaherpesvirus-68 LatencyR01CA095318 · NCI · EMORY UNIVERSITY · PI SCHARER, CHRISTOPHER D · 2003 to 2019
$4.9M
Control of Gammaherpesvirus ReplicationR01CA052004 · NCI · WASHINGTON UNIVERSITY · PI SPECK, SAMUEL H · 1990 to 2013
$4.1M
REGULATION OF EBV TRANSCRIPTION IN BURKITTS LYMPHOMAR01CA058524 · NCI · WASHINGTON UNIVERSITY · PI SPECK, SAMUEL H · 1995 to 2009
$2.4M
NCI NIH HHS R01 CA052004NCI NIH HHS R01 CA058524NCI NIH HHS R01 CA095318NCI NIH HHS R01 CA52004NCI NIH HHS R01 CA58524NCI NIH HHS R01 CA95318NIAID NIH HHS R01 AI05807
6 · The paper itself

Abstract

Gammaherpesvirus 68 (gammaHV68, or MHV68) is a naturally occurring rodent pathogen that replicates to high titer in cell culture and is amenable to in vivo experimental evaluation of viral and host determinants of gammaherpesvirus disease. However, the inability of MHV68 to transform primary murine B cells in culture, the absence of a robust cell culture latency system, and the paucity of MHV68-positive tumor cell lines have limited an understanding of the molecular mechanisms by which MHV68 modulates the host cell during latency and reactivation. To facilitate a more complete understanding of viral and host determinants that regulate MHV68 latency and reactivation in B cells, we generated a recombinant MHV68 virus that encodes a hygromycin resistance protein fused to enhanced green fluorescent protein as a means to select cells in culture that harbor latent virus. We utilized this virus to infect the A20 murine mature B-cell line and evaluate reactivation competence following treatment with diverse stimuli to reveal viral gene expression, DNA replication, and production of progeny virions. Comparative analyses of parental and infected A20 cells indicated a correlation between infection and alterations in DNA damage signaling following etoposide treatment. The data described in this study highlight the potential utility of this new cell culture-based system to dissect molecular mechanisms that regulate MHV68 latency and reactivation, as well as having the potential of illuminating biochemical alterations that contribute to gammaherpesvirus pathogenesis. In addition, such cell lines may be of value in evaluating targeted therapies to gammaherpesvirus-related tumors.

Indexed as

DNA DamageSignal TransductionAnimalsAntineoplastic Agents, PhytogenicB-LymphocytesCell LineEtoposideMiceProvirusesRhadinovirusVirologyVirus ActivationVirus LatencyAntineoplastic Agents, PhytogenicEtoposide

Identifiers

PMID18495760
PMCPMC2493333
OpenAlexW2066610233

What OpenQuestion holds

Textmetadata
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.