Evidence map›Paper›PMID 12134023›Full record

ArticleJournal of virology2002

The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules.

Sinéad Keating, Stuart Prince, Matthew Jones, Martin Rowe

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Structurally diverse viral inhibitors converge on a shared mechanism to stall the antigen transporter TAP.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. A Structural Atlas of TAP Inhibition by Herpesviruses and Poxviruses.bioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Viruses in colorectal cancer.Molecular oncology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Epstein-Barr Virus and Multiple Sclerosis.Frontiers in immunology · 2020
    Review
  13. Epstein-Barr Virus and the Human Leukocyte Antigen Complex.Current clinical microbiology reports · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

Sinéad KeatingSection of Infection and Immunity, University of Wales College of Medicine, Cardiff CF14 4XX, United Kingdom.
Stuart Prince
Matthew Jones
Martin Rowe
University of Wales · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Human herpesviruses utilize an impressive range of strategies to evade the immune system during their lytic replicative cycle, including reducing the expression of cell surface major histocompatibility complex (MHC) and immunostimulatory molecules required for recognition and lysis by virus-specific cytotoxic T cells. Study of possible immune evasion strategies by Epstein-Barr virus (EBV) in lytically infected cells has been hampered by the lack of an appropriate permissive culture model. Using two-color immunofluorescence staining of cell surface antigens and EBV-encoded lytic cycle antigens, we examined EBV-transformed B-cell lines in which a small subpopulation of cells had spontaneously entered the lytic cycle. Cells in the lytic cycle showed a four- to fivefold decrease in cell surface expression of MHC class I molecules relative to that in latently infected cells. Expression of MHC class II molecules, CD40, and CD54 was reduced by 40 to 50% on cells in the lytic cycle, while no decrease was observed in cell surface expression of CD19, CD80, and CD86. Downregulation of MHC class I expression was found to be an early-lytic-cycle event, since it was observed when progress through late lytic cycle was blocked by treatment with acyclovir. The immediate-early transactivator of the EBV lytic cycle, BZLF1, did not directly affect expression of MHC class I molecules. However, BZLF1 completely inhibited the upregulation of MHC class I expression mediated by the EBV cell-transforming protein, LMP1. This novel function of BZLF1 elucidates the paradox of how MHC class I expression can be downregulated when LMP1, which upregulates MHC class I expression in latent infection, remains expressed in the lytic cycle.

Indexed as

Viral ProteinsAntigen PresentationCell Line, TransformedDNA-Binding ProteinsDown-RegulationHerpesvirus 4, HumanHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHumansNF-kappa BT-Lymphocytes, CytotoxicTrans-ActivatorsViral Matrix ProteinsBZLF1 protein, Herpesvirus 4, HumanDNA-Binding ProteinsEBV-associated membrane antigen, Epstein-Barr virusHistocompatibility Antigens Class IHistocompatibility Antigens Class IINF-kappa BTrans-ActivatorsViral Matrix ProteinsViral Proteins

Identifiers

PMID12134023
PMCPMC155144
OpenAlexW2139718667

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.