Evidence map›Paper›PMID 18596690›Full record

ArticleNature2008

MicroRNAs expressed by herpes simplex virus 1 during latent infection regulate viral mRNAs.

Jennifer Lin Umbach, Martha F Kramer, Igor Jurak, Heather W Karnowski, Donald M Coen, Bryan R Cullen

Open access · greenAbstract read
In one paragraph

Article in Nature, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 445 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
445citing papers in PubMed, 1 pooled it
37.5field-weighted citation impact, top 1% 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

445 citing papers in PubMed, 1 synthesis or guideline pooled it, 689 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
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  20. Review

385 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Jennifer Lin UmbachDepartment of Molecular Genetics and Microbiology and Center for Virology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Martha F Kramer
Igor Jurak
Heather W Karnowski
Donald M Coen
Bryan R Cullen
Harvard University · USDuke Medical Center · USDuke University · US

Funding

Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
Role and mechanism of action of Gamma herpesvirus microRNAsR01AI067968 · NIAID · DUKE UNIVERSITY · PI CULLEN, BRYAN R. · 2006 to 2016
$3.6M
NCI NIH HHS T32 CA009111NIAID NIH HHS R01 AI067968
6 · The paper itself

Abstract

Herpesviruses are characterized by their ability to maintain life-long latent infections in their animal hosts. However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT). Here we show that LAT functions as a primary microRNA (miRNA) precursor that encodes four distinct miRNAs in HSV-1 infected cells. One of these miRNAs, miR-H2-3p, is transcribed in an antisense orientation to ICP0-a viral immediate-early transcriptional activator that is important for productive HSV-1 replication and thought to have a role in reactivation from latency. We show that miR-H2-3p is able to reduce ICP0 protein expression, but does not significantly affect ICP0 messenger RNA levels. We also identified a fifth HSV-1 miRNA in latently infected trigeminal ganglia, miR-H6, which derives from a previously unknown transcript distinct from LAT. miR-H6 shows extended seed complementarity to the mRNA encoding a second HSV-1 transcription factor, ICP4, and inhibits expression of ICP4, which is required for expression of most HSV-1 genes during productive infection. These results may explain the reported ability of LAT to promote latency. Thus, HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression.

Indexed as

Gene Expression Regulation, ViralAnimalsBase SequenceCell LineDown-RegulationGenome, ViralHerpesvirus 1, HumanHumansImmediate-Early ProteinsMaleMiceMicroRNAsRNA, MessengerRNA Processing, Post-TranscriptionalRNA, ViralUbiquitin-Protein Ligasesherpes simplex virus, type 1 protein ICP4Immediate-Early Proteinslatency associated transcript, herpes simplex virus-1MicroRNAsRNA, MessengerRNA, ViralUbiquitin-Protein LigasesVmw110 protein, Human herpesvirus 1

Identifiers

PMID18596690
PMCPMC2666538
OpenAlexW2056295530

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.