Evidence map›Paper›PMID 11238834›Full record

ArticleJournal of virology2001

Herpes simplex virus-induced keratitis: evaluation of the role of molecular mimicry in lesion pathogenesis.

S P Deshpande, S Lee, M Zheng, B Song, D Knipe, J A Kapp, B T Rouse

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. CXCL17 Chemokine-Dependent Mobilization of CXCR8Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  8. Review
  9. Review
  10. Herpes keratitis.Progress in retinal and eye research · 2013
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Anti-retinal autoantibodies in experimental ocular and systemic toxoplasmosis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2010
    Article
  16. Review
  17. Article
  18. Herpes keratitis in the absence of anterograde transport of virus from sensory ganglia to the cornea.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  19. Homing in on the cellular immune response to HSV-2 in humans.American journal of reproductive immunology (New York, N.Y. : 1989) · 2005
    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

7 authors at 3 institutions in 1 country.

S P DeshpandeDepartment of Microbiology, University of Tennessee, Knoxville, Tennessee 37996, USA.
S Lee
M Zheng
B Song
D Knipe
J A Kapp
B T Rouse
University of Tennessee at Knoxville · USHarvard University · USEmory University · US

Funding

P30-Core Grant for Vision Research Core CP30EY006360 · NEI · EMORY UNIVERSITY · PI NICKERSON, JOHN M · 1986 to 2025
$15.3M
Mechanisms of Herpetic KeratitisR01EY005093 · NEI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ROUSE, BARRY T. · 1985 to 2020
$7.8M
NEI NIH HHS EY05093NEI NIH HHS P30 EY006360NEI NIH HHS P30 EYO 06360NEI NIH HHS R01 EY005093
6 · The paper itself

Abstract

Viruses are suspected but usually unproven triggering factors in autoimmunity. One favored mechanism to explain the role of viruses in the genesis of autoimmunity is molecular mimicry. An immunoinflammatory blinding lesion called herpetic stromal keratitis (HSK) that follows ocular infection with herpes simplex virus (HSV) is suggested to result from a CD4(+) T-cell response to a UL6 peptide of HSV that cross-reacts with a corneal autopeptide shared with the immunoglobulin G2a(b) (IgG2a(b)) isotype. The present report reevaluates the molecular mimicry hypothesis to explain HSK pathogenesis. Our results failed to reveal cross-reactivity between the UL6 and IgG2a(b) peptides or between peptide reactive T cells and HSV antigens. More importantly, animals infected with HSV failed to develop responses that reacted with either peptide, and infection with a recombinant vaccinia UL6 vector failed to cause HSK, in spite of generating UL6 reactivity. Other lines of evidence also failed to support the molecular mimicry hypothesis, such as the failure to affect HSK severity upon tolerization of susceptible BALB/c and B-cell-deficient mice with IgG2a(b) or UL6 peptides. An additional study system revealed that HSK could be induced in mouse strains, such as the OT2 x RAG1(-/-) mice (T cell receptor transgenic recognizing OVA(323-339)) that were unable to produce CD4(+) T-cell responses to any detectable HSV antigens. Our results cast doubt on the molecular mimicry hypothesis as an explanation for the pathogenesis of HSK and indicate that if autoimmunity is involved its likely proceeds via a bystander activation mechanism.

Indexed as

Capsid ProteinsAnimalsAutoimmune DiseasesCapsidCross ReactionsGenetic Predisposition to DiseaseHerpesvirus 1, HumanImmunoglobulin GImmunoglobulin Heavy ChainsKeratitis, HerpeticMiceMice, SCIDViral ProteinsCapsid ProteinsDNA cleavage and packaging proteins, HerpesvirusImmunoglobulin GImmunoglobulin Heavy ChainsViral Proteins

Identifiers

PMID11238834
PMCPMC114101
OpenAlexW2117825322

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.