Evidence map›Paper›PMID 27357149›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Resident T Cells Are Unable To Control Herpes Simplex Virus-1 Activity in the Brain Ependymal Region during Latency.

Chandra M Menendez, Jeremy K Jinkins, Daniel J J Carr

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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
4.5field-weighted citation impact, top 5% 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, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Immune Modulatory Effects of Vitamin D on Herpesvirus Infections.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. The Adult Neurogenesis Theory of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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 at 1 institution in 1 country.

Chandra M MenendezDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; and.
Jeremy K JinkinsDepartment of Ophthalmology, Dean A. McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104.
Daniel J J CarrDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104; and Department of Ophthalmology, Dean A. McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104 dan-carr@ouhsc.edu.
University of Oklahoma Health Sciences Center · US

Funding

P30-CENTER CORE GRANT FOR VISION RESEARCHP30EY021725 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Michelle C Callegan · 2011 to 2026
$10.5M
The Neuroimmunology of Viral InfectionR01AI053108 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CARR, DANIEL J · 2003 to 2022
$5.8M
Molecular Basis of Immunity - Kirschtein-NRSAT32AI007633 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 2001 to 2022
$4.0M
NEI NIH HHS P30 EY021725NIAID NIH HHS HHSN272201300006CNIAID NIH HHS R01 AI053108NIAID NIH HHS T32 AI007633
6 · The paper itself

Abstract

HSV type 1 (HSV-1) is one of the leading etiologies of sporadic viral encephalitis. Early antiviral intervention is crucial to the survival of herpes simplex encephalitis patients; however, many survivors suffer from long-term neurologic deficits. It is currently understood that HSV-1 establishes a latent infection within sensory peripheral neurons throughout the life of the host. However, the tissue residence of latent virus, other than in sensory neurons, and the potential pathogenic consequences of latency remain enigmatic. In the current study, we characterized the lytic and latent infection of HSV-1 in the CNS in comparison with the peripheral nervous system following ocular infection in mice. We used RT-PCR to detect latency-associated transcripts and HSV-1 lytic cycle genes within the brain stem, the ependyma (EP), containing the limbic and cortical areas, which also harbor neural progenitor cells, in comparison with the trigeminal ganglia. Unexpectedly, HSV-1 lytic genes, usually identified during acute infection, are uniquely expressed in the EP 60 d postinfection when animals are no longer suffering from encephalitis. An inflammatory response was also mounted in the EP by the maintenance of resident memory T cells. However, EP T cells were incapable of controlling HSV-1 infection ex vivo and secreted less IFN-γ, which correlated with expression of a variety of exhaustion-related inhibitory markers. Collectively, our data suggest that the persistent viral lytic gene expression during latency is the cause of the chronic inflammatory response leading to the exhaustion of the resident T cells in the EP.

Indexed as

AnimalsDisease Models, AnimalEncephalitis, Herpes SimplexEpendymaFlow CytometryHerpes SimplexHerpesvirus 1, HumanMiceMice, Inbred C57BLMice, TransgenicReal-Time Polymerase Chain ReactionT-LymphocytesVirus Latency

Identifiers

PMID27357149
PMCPMC4975964
OpenAlexW2466478581

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.