Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1–infected lymphocytes

Cell-cell contact is required for efficient transmission of human T-lymphotropic virus type 1 (HTLV-910101). An HTLV-1–infected cell polarizes its microtubule-organizing center (MTOC) toward the cell-cell junction; HTLV-1 core (Gag) complexes and the HTLV-1 genome accumulate at the point of contact...

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Bibliographic Details
Published in:Blood 2005-08, Vol.106 (3), p.988-995
Main Authors: Barnard, Amanda L., Igakura, Tadahiko, Tanaka, Yuetsu, Taylor, Graham P., Bangham, Charles R.M.
Format: Article
Language:English
Subjects:
Biological and medical sciences
CD4-Positive T-Lymphocytes - chemistry
CD4-Positive T-Lymphocytes - physiology
CD4-Positive T-Lymphocytes - virology
Cell Adhesion Molecules - physiology
Cell Communication
Cell Polarity - physiology
Cells, Cultured
Cytoskeleton - metabolism
Cytoskeleton - virology
Gene Products, tax - physiology
HTLV-I Infections - etiology
Human T-lymphotropic virus 1 - genetics
Human T-lymphotropic virus 1 - physiology
Human viral diseases
Humans
Infectious diseases
Intercellular Adhesion Molecule-1 - biosynthesis
Intercellular Adhesion Molecule-1 - genetics
Intercellular Adhesion Molecule-1 - physiology
Medical sciences
Microtubule-Organizing Center - physiology
Microtubule-Organizing Center - virology
Up-Regulation - genetics
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
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Summary:Cell-cell contact is required for efficient transmission of human T-lymphotropic virus type 1 (HTLV-910101). An HTLV-1–infected cell polarizes its microtubule-organizing center (MTOC) toward the cell-cell junction; HTLV-1 core (Gag) complexes and the HTLV-1 genome accumulate at the point of contact and are then transferred to the uninfected cell. However, the mechanisms involved in this cytoskeletal polarization and transport of HTLV-1 complexes are unknown. Here, we tested the hypothesis that engagement of a specific T-cell surface ligand is synergistic with HTLV-1 infection in causing polarization of the MTOC to the cell contact region. We show that antibodies to intercellular adhesion molecule-1 (ICAM-1; CD54) caused MTOC polarization at a higher frequency in HTLV-1–infected cells. ICAM-1 is upregulated on HTLV-1–infected cells, and, in turn, ICAM-1 on the cell surface upregulates HTLV-1 gene expression. We propose that a positive feedback loop involving ICAM-1 and HTLV-1 Tax protein facilitates the formation of the virologic synapse and contributes to the T-cell tropism of HTLV-1. In contrast, MTOC polarization induced in T cells by antibodies to CD3 or CD28 was significantly inhibited by HTLV-1 infection.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood-2004-07-2850