Evidence map›Paper›PMID 20573821›Full record

ArticleJournal of virology2010

Delaying the expression of herpes simplex virus type 1 glycoprotein B (gB) to a true late gene alters neurovirulence and inhibits the gB-CD8+ T-cell response in the trigeminal ganglion.

Srividya Ramachandran, Katherine A Davoli, Michael B Yee, Robert L Hendricks, Paul R Kinchington

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2010. 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
2.1field-weighted citation impact, top 13% 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, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Inhibiting Glucose Metabolism Results in Herpes Simplex Encephalitis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Herpes Simplex Virus 1-Specific CD8Journal of virology · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Srividya RamachandranDepartment of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Katherine A Davoli
Michael B Yee
Robert L Hendricks
Paul R Kinchington
University of Pittsburgh · US

Funding

Virus Production and Manipulation of Protein/Gene Expression ModuleP30EY008098 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Ian A Sigal · 1989 to 2026
$17.8M
ROLE OF CYTOTOXIC LYMPHOCYTES IN HSV-1 CORNEAL LESIONSR01EY005945 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HENDRICKS, ROBERT L · 1986 to 2017
$8.3M
Gene Expression in HSV-1 Latency After Corneal InfectionR01EY015291 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KINCHINGTON, PAUL R. · 2004 to 2013
$2.9M
NEI NIH HHS EY015291NEI NIH HHS EY05945NEI NIH HHS EY08098NEI NIH HHS P30 EY008098NEI NIH HHS R01 EY005945NEI NIH HHS R01 EY015291
6 · The paper itself

Abstract

Following herpes simplex virus type 1 (HSV-1) ocular infection of C57BL/6 mice, activated CD8(+) T cells specific for an immunodominant epitope on HSV-1 glycoprotein B (gB-CD8 cells) establish a stable memory population in HSV-1 latently infected trigeminal ganglia (TG), whereas non-HSV-specific CD8(+) T cells are lost over time. The retention and activation of gB-CD8 cells appear to be influenced by persistent viral antigenic exposure within the latently infected TG. We hypothesized that the low-level expression of gB from its native promoter before viral DNA synthesis is critical for the retention and activation of gB-CD8 cells in the TG during HSV-1 latency and for their ability to block HSV-1 reactivation from latency. To test this, we created a recombinant HSV-1 in which gB is expressed only after viral DNA synthesis from the true late gC promoter (gCp-gB). Despite minor growth differences compared to its rescuant in infected corneas, gCp-gB was significantly growth impaired in the TG and produced a reduced latent genome load. The gCp-gB- and rescuant-infected mice mounted similar gB-CD8 effector responses, but the size and activation phenotypes of the memory gB-CD8 cells were diminished in gCp-gB latently infected TG, suggesting that the stimulation of gB-CD8 cells requires gB expression before viral DNA synthesis. Surprisingly, late gB expression did not compromise the capacity of gB-CD8 cells to inhibit HSV-1 reactivation from latency in ex vivo TG cultures, suggesting that gB-CD8 cells can block HSV-1 reactivation at a very late stage in the viral life cycle. These data have implications for designing better immunogens for vaccines to prevent HSV-1 reactivation.

Indexed as

Gene Expression Regulation, ViralAnimalsCD8-Positive T-LymphocytesChlorocebus aethiopsFemaleHerpes SimplexHerpesvirus 1, HumanHumansMiceMice, Inbred C57BLTrigeminal GanglionVero CellsViral Envelope ProteinsVirulenceglycoprotein B, SimplexvirusViral Envelope Proteins

Identifiers

PMID20573821
PMCPMC2919033
OpenAlexW2162510249

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.