Evidence map›Paper›PMID 12857897›Full record

ArticleJournal of virology2003

Pathogenic effects of human herpesvirus 6 in human lymphoid tissue ex vivo.

Jean-Charles Grivel, Fabio Santoro, Silvia Chen, Giovanni Fagá, Mauro S Malnati, Yoshinori Ito, Leonid Margolis, Paolo Lusso

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Lymphoproliferative Syndromes Associated with Human Herpesvirus-6A and Human Herpesvirus-6B.Mediterranean journal of hematology and infectious diseases · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
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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

8 authors at 2 institutions in 2 countries.

Jean-Charles GrivelLaboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Fabio Santoro
Silvia Chen
Giovanni Fagá
Mauro S Malnati
Yoshinori Ito
Leonid Margolis
Paolo Lusso
National Institutes of Health · USUniversity of Cagliari · IT

Funding

Cell Interactions in Three Dimensional Tissue CultureZIAHD001416 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MARGOLIS, LEONID B. · 2009 to 2017
$15.7M
TISSUE IMAGING IN CELL BIOLOGYZ01HD001416 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MARGOLIS, LEONID B. · 1993 to 2008
$2.7M
6 · The paper itself

Abstract

Human herpesvirus 6 (HHV-6) is a potentially immunosuppressive agent that has been suggested to act as a cofactor in the progression of human immunodeficiency virus disease. However, the lack of suitable experimental models has hampered the elucidation of the mechanisms of HHV-6-mediated immune suppression. Here, we used ex vivo lymphoid tissue to investigate the cellular tropism and pathogenic mechanisms of HHV-6. Viral strains belonging to both HHV-6 subgroups (A and B) were able to productively infect human tonsil tissue fragments in the absence of exogenous stimulation. The majority of viral antigen-expressing cells were CD4(+) T lymphocytes expressing a nonnaive phenotype, while CD8(+) T cells were efficiently infected only with HHV-6A. Accordingly, HHV-6A infection resulted in the depletion of both CD4(+) and CD8(+) T cells, whereas in HHV-6B-infected tissue CD4(+) T cells were predominantly depleted. The expression of different cellular antigens was dramatically altered in HHV-6-infected tissues: whereas CD4 was upregulated, both CD46, which serves as a cellular receptor for HHV-6, and CD3 were downmodulated. However, CD3 downmodulation was restricted to infected cells, while the loss of CD46 expression was generalized. Moreover, HHV-6 infection markedly enhanced the production of the CC chemokine RANTES, whereas other cytokines and chemokines were only marginally affected. These results provide the first evidence, in a physiologically relevant study model, that HHV-6 can severely affect the physiology of secondary lymphoid organs through direct infection of T lymphocytes and modulation of key membrane receptors and chemokines.

Indexed as

Antigens, CDCD3 ComplexCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesChemokine CCL5Culture TechniquesDown-RegulationFlow CytometryHerpesvirus 6, HumanHumansMembrane Cofactor ProteinMembrane GlycoproteinsPalatine TonsilRoseolovirus InfectionsUp-RegulationVirus ReplicationAntigens, CDCD3 ComplexCD46 protein, humanChemokine CCL5Membrane Cofactor ProteinMembrane Glycoproteins

Identifiers

PMID12857897
PMCPMC165251
OpenAlexW2050089095

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.