The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Valentin, A.
Right arrow Articles by Asjo, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Valentin, A.
Right arrow Articles by Asjo, B.

The Journal of Immunology, Vol 144, Issue 3 934-937, Copyright © 1990 by American Association of Immunologists

ARTICLES

The leukocyte adhesion glycoprotein CD18 participates in HIV-1-induced syncytia formation in monocytoid and T cells

A Valentin, K Lundin, M Patarroyo and B Asjo
Department of Virology, Karolinska Institute, Stockholm, Sweden.

mAb 60.3 and IB4 to CD18, the common beta-subunit of the human leukocytic cell adhesion molecule family, efficiently inhibit syncytium formation induced by the interaction of HIV type 1 (HIV-1)-infected monocytoid cells and CD4+ T cells. The antibodies also interfere with cellfree HIV-1 infection of U-937 clone 16 cells. Virus-induced aggregation of these cells and the subsequent syncytia formation leading to massive cell death are efficiently blocked, and the number of infected cells remains at a very low level, 2 to 5%, for the entire culture period. However, anti-CD18 mAb do not inhibit binding of the viral envelope glycoprotein gp120 to the cell surface receptor CD4. The results indicate participation of CD18, or of the protein complex CD11a- c/CD18, in addition to CD4, in the infection and cytopathic effect of HIV-1. They also suggest that intercellular adhesion contributes to virus transmission from cell to cell and may be an important mechanism for virus spreading.


This article has been cited by other articles:


Home page
 J. Virol.Home page
R. Tanaka, A. Yoshida, T. Murakami, E. Baba, J. Lichtenfeld, T. Omori, T. Kimura, N. Tsurutani, N. Fujii, Z.-X. Wang, et al.
Unique Monoclonal Antibody Recognizing the Third Extracellular Loop of CXCR4 Induces Lymphocyte Agglutination and Enhances Human Immunodeficiency Virus Type 1-Mediated Syncytium Formation and Productive Infection
J. Virol., December 1, 2001; 75(23): 11534 - 11543.
[Abstract] [Full Text]

Home page
 J. Leukoc. Biol.Home page
K. Mizuno, H. Okamoto, and T. Horio
Muramyl dipeptide and mononuclear cell supernatant induce Langhans-type cells from human monocytes
J. Leukoc. Biol., September 1, 2001; 70(3): 386 - 394.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
S. Lagaye, M. Derrien, E. Menu, C. Coïto, E. Tresoldi, P. Mauclère, G. Scarlatti, G. Chaouat, F. Barré-Sinoussi, M. Bomsel, et al.
Cell-to-Cell Contact Results in a Selective Translocation of Maternal Human Immunodeficiency Virus Type 1 Quasispecies across a Trophoblastic Barrier by both Transcytosis and Infection
J. Virol., May 15, 2001; 75(10): 4780 - 4791.
[Abstract] [Full Text]

Home page
 J. Virol.Home page
B. Barbeau, J.-F. Fortin, N. Genois, and M. J. Tremblay
Modulation of Human Immunodeficiency Virus Type 1-Induced Syncytium Formation by the Conformational State of LFA-1 Determined by a New Luciferase-Based Syncytium Quantitative Assay
J. Virol., September 1, 1998; 72(9): 7125 - 7136.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1990 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1990 by The American Association of Immunologists, Inc. All rights reserved.