Evidence map›Paper›PMID 29250481›Full record

ArticleCurrent clinical microbiology reports2017

The loss of binary: Pushing the herpesvirus latency paradigm.

Donna Collins-McMillen, Felicia D Goodrum

Open access · greenAbstract read
In one paragraph

Article in Current clinical microbiology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Viral gene drive in herpesviruses.Nature communications · 2020
    Article
  16. Control of Immediate Early Gene Expression for Human Cytomegalovirus Reactivation.Frontiers in cellular and infection microbiology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. CNS infection and immune privilege.Nature reviews. Neuroscience · 2018
    Review
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.

Donna Collins-McMillenBIO5 Institute, University of Arizona, Tucson, AZ, USA.
Felicia D GoodrumBIO5 Institute, University of Arizona, Tucson, AZ, USA.
University of Arizona · US

Funding

Mechanisms of Human Cytomegalovirus Latency in Primary Human Hematopoietic CellsR01AI079059 · NIAID · UNIVERSITY OF ARIZONA · PI GOODRUM, FELICIA D · 2008 to 2018
$4.4M
Mechanisms of Human Cytomegalovirus Latency in Primary Human Hematopoietic CellsR37AI079059 · NIAID · UNIVERSITY OF ARIZONA · PI Felicia D Goodrum · 2019 to 2026
$3.3M
Antagonistic Viral Determinants Regulating the Outcome of InfectionR56AI105062 · NIAID · UNIVERSITY OF ARIZONA · PI GOODRUM, FELICIA D · 2013 to 2013
$380k
NIAID NIH HHS R01 AI079059NIAID NIH HHS R37 AI079059NIAID NIH HHS R56 AI105062
6 · The paper itself

Abstract

purpose of reviewHerpesvirus latency has been viewed as a binary state where replication is either on or off. During latency, gene expression is thought to be restricted to non-coding RNAs or very few proteins so that the virus avoids detection by the immune system. However, a number of recent studies across herpesvirus families call into question the existence of a binary switch for latency, and suggest that latency is far more dynamic than originally presumed. These studies are the focus of this review. RECENT

findingsHighly sensitive and global approaches to investigate viral gene expression in the context of latency have revealed low level viral transcripts, and in some cases protein, from each of the three kinetic gene classes during the latent alpha and beta herpesvirus infection either SUMMARY: Emerging evidence suggests that viral gene expression associated with latent states may be broader and more dynamic than originally presumed during herpesvirus latency. This is an important possibility to consider in understanding the molecular programs associated with the establishment, maintenance and reactivation of herpesvirus latency. Here, we review these findings and detail how they contribute to the emergence of a biphasic model of reactivation.

Indexed as

cytomegalovirusherpes simplex virusherpesviruslatencyreactivation

Identifiers

PMID29250481
PMCPMC5726573
OpenAlexW2748316465

What OpenQuestion holds

Textmetadata
LicenceTDM
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.