Evidence map›Paper›PMID 28594343›Full record

ArticlePathogens (Basel, Switzerland)2017

Modeling HSV-1 Latency in Human Embryonic Stem Cell-Derived Neurons.

Aldo Pourchet, Aram S Modrek, Dimitris G Placantonakis, Ian Mohr, Angus C Wilson

Open access · goldAbstract read
In one paragraph

Article in Pathogens (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Using 2D and 3D pluripotent stem cell models to study neurotropic viruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Aldo PourchetDepartment of Microbiology, New York University School of Medicine, New York, NY 10016, USA. pourchet@upenn.edu.
Aram S ModrekDepartment of Neurosurgery, New York University School of Medicine, New York, NY 10016, USA. Aram.Modrek@med.nyu.edu.
Dimitris G PlacantonakisDepartment of Neurosurgery, New York University School of Medicine, New York, NY 10016, USA. Dimitris.Placantonakis@nyumc.org.
Ian MohrDepartment of Microbiology, New York University School of Medicine, New York, NY 10016, USA. Ian.Mohr@med.nyu.edu.
Angus C WilsonDepartment of Microbiology, New York University School of Medicine, New York, NY 10016, USA. angus.wilson@med.nyu.edu.
New York University · US

Funding

Project-005UL1TR001445 · NCATS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BREDELLA, MIRIAM ANTOINETTE, HOCHMAN, JUDITH S · 2015 to 2025
$103.5M
New tools to study the dynamics of HSV latency and reactivation in living neuronsR21AI103933 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MOHR, IAN J, WILSON, ANGUS C · 2013 to 2014
$451k
Metabolic aberrations in glioma initiationR03NS087349 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NEUBERT, THOMAS A, PLACANTONAKIS, DIMITRIS G. · 2015 to 2016
$170k
NCATS NIH HHS UL1 TR001445NIAID NIH HHS R21 AI103933NINDS NIH HHS R03 NS087349
6 · The paper itself

Abstract

Herpes simplex virus 1 (HSV-1) uses latency in peripheral ganglia to persist in its human host, however, recurrent reactivation from this reservoir can cause debilitating and potentially life-threatening disease. Most studies of latency use live-animal infection models, but these are complex, multilayered systems and can be difficult to manipulate. Infection of cultured primary neurons provides a powerful alternative, yielding important insights into host signaling pathways controlling latency. However, small animal models do not recapitulate all aspects of HSV-1 infection in humans and are limited in terms of the available molecular tools. To address this, we have developed a latency model based on human neurons differentiated in culture from an NIH-approved embryonic stem cell line. The resulting neurons are highly permissive for replication of wild-type HSV-1, but establish a non-productive infection state resembling latency when infected at low viral doses in the presence of the antivirals acyclovir and interferon-α. In this state, viral replication and expression of a late viral gene marker are not detected but there is an accumulation of the viral latency-associated transcript (LAT) RNA. After a six-day establishment period, antivirals can be removed and the infected cultures maintained for several weeks. Subsequent treatment with sodium butyrate induces reactivation and production of new infectious virus. Human neurons derived from stem cells provide the appropriate species context to study this exclusively human virus with the potential for more extensive manipulation of the progenitors and access to a wide range of preexisting molecular tools.

Indexed as

alphaherpesvirusembryonic stem cellsherpes simplex virusHSV-1humanlatencyprimary neuronsreactivation

Identifiers

PMID28594343
PMCPMC5488658
OpenAlexW2623595296

What OpenQuestion holds

Textmetadata
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.