Circulating Intercellular Adhesion Molecule-1 in Human Immunodeficiency Virus Infection

1994 ◽  
Vol 169 (5) ◽  
pp. 1176-1176 ◽  
Author(s):  
Antonio Aceti ◽  
Arrigo Benedetto ◽  
Antonio Sebastiani
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Immunodeficiency Virus

scholarly journals Statin Compounds Reduce Human Immunodeficiency Virus Type 1 Replication by Preventing the Interaction between Virion-Associated Host Intercellular Adhesion Molecule 1 and Its Natural Cell Surface Ligand LFA-1

2004 ◽  
Vol 78 (21) ◽  
pp. 12062-12065 ◽  
Author(s):  
Jean-François Giguère ◽  
Michel J. Tremblay
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT A variety of host factors, including membrane proteins acquired by human immunodeficiency virus type 1 (HIV-1), play a dominant role in HIV-1 adsorption onto host cells. Examples include the integrin intercellular adhesion molecule 1 (ICAM-1), which, once acquired by HIV-1, promotes virus infectivity via ligation to LFA-1. We tested the ability of statins to diminish HIV-1 replication, based on the idea that these compounds have been shown to block ICAM-1-LFA-1 interactions. Our data indicate that statins diminish HIV-1 attachment to target cells by suppressing ICAM-1-LFA-1 interactions. The capacity of statins to limit the initial steps in virus replication could represent an interesting approach for the treatment of HIV-1 infection.

scholarly journals Binding of LFA-1 (CD11a) to Intercellular Adhesion Molecule 3 (ICAM-3; CD50) and ICAM-2 (CD102) Triggers Transmigration of Human Immunodeficiency Virus Type 1-Infected Monocytes through Mucosal Epithelial Cells

2002 ◽  
Vol 76 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Marie-Paule Carreno ◽  
Nicolas Chomont ◽  
Michel D. Kazatchkine ◽  
Theano Irinopoulou ◽  
Corrine Krief ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Mononuclear Cells ◽  
Sexual Transmission ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Transmigration of human immunodeficiency virus (HIV)-infected mononuclear cells through the genital mucosa is one of the possible mechanisms of sexual transmission of HIV. Here, we investigated the transmigration of cell-associated R5-tropic HIV type 1 (HIV-1) through a tight monolayer of human epithelial cells in vitro. We show that this process is dependent on an initial interaction between αLβ2 integrin CD11a/CD18 on infected monocytic cells and intercellular adhesion molecule 2 (ICAM-2; CD102) and ICAM-3 (CD50) on the apical membrane of epithelial cells. The CD50 and CD102 ligands were overexpressed on epithelial cells when the cells were activated by proinflammatory cytokines in the cellular microenvironment. An accumulation of proviral DNA was found in the transmigrated cells, clearly reflecting the preferential transepithelial migration of HIV-1-infected cells under proinflammatory conditions. Our observations provide new insights supporting the hypothesis that HIV-infected mononuclear cells contained in genital secretions from infected individuals may cross the epithelial genital mucosa of an exposed receptive sexual partner, particularly under inflammatory conditions of damaged genital tissue. Understanding the fundamental aspects of the initial HIV entry process during sexual transmission remains a critical step for preventing human infection and developing further vaccinal strategies and virucidal agents.

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