Evidence map›Paper›PMID 10846084›Full record

ArticleJournal of virology2000

Interactions between brain endothelial cells and human T-cell leukemia virus type 1-infected lymphocytes: mechanisms of viral entry into the central nervous system.

I A Romero, M C Prevost, E Perret, P Adamson, J Greenwood, P O Couraud, S Ozden

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Article
  3. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Central nervous system niche involvement in the leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Neuroimmunity of HTLV-I Infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  17. Review
  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

7 authors at 3 institutions in 2 countries.

I A RomeroCNRS UPR 0415, Institut Cochin de Génétique Moléculaire, 75014 Paris, France. i.romero@open.ac.uk
M C Prevost
E Perret
P Adamson
J Greenwood
P O Couraud
S Ozden
Centre National de la Recherche Scientifique · FRInstitute of Ophthalmology · MXInstitut Cochin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is associated with a variety of clinical manifestations, including tropical spastic paraparesis or HTLV-1-associated myelopathy (TSP/HAM). Viral detection in the central nervous system (CNS) of TSP/HAM patients demonstrates the ability of HTLV-1 to cross the blood-brain barrier (BBB). To investigate viral entry into the CNS, rat brain capillary endothelial cells were exposed to human lymphocytes chronically infected by HTLV-1 (MT2), to lymphocytes isolated from a seropositive patient, or to a control lymphoblastoid cell line (CEM). An enhanced adhesion to and migration through brain endothelial cells in vitro was observed with HTLV-1-infected lymphocytes. HTLV-1-infected lymphocytes also induced a twofold increase in the paracellular permeability of the endothelial monolayer. These effects were associated with an increased production of tumor necrosis factor alpha by HTLV-1-infected lymphocytes in the presence of brain endothelial cells. Ultrastructural analysis showed that contact between endothelial cells and HTLV-1-infected lymphocytes resulted in a massive and rapid budding of virions from lymphocytes, followed by their internalization into vesicles by brain endothelial cells and apparent release onto the basolateral side, suggesting that viral particles may cross the BBB using the transcytotic pathway. Our study also demonstrates that cell-cell fusion occurs between HTLV-1-infected lymphocytes and brain endothelial cells, with the latter being susceptible to transient HTLV-1 infection. These aspects may help us to understand the pathogenic mechanisms associated with neurological diseases induced by HTLV-1 infection.

Indexed as

AnimalsBrainCapillariesCell AdhesionCell FusionCell Membrane PermeabilityCell MovementCells, CulturedCentral Nervous SystemCoculture TechniquesEndocytosisEndothelium, VascularHumansHuman T-lymphotropic virus 1Integrin alpha4beta1IntegrinsIntegrin alpha4beta1IntegrinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Receptors, Lymphocyte HomingTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID10846084
PMCPMC112099
OpenAlexW2119329692

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.