Antibody-dependent enhancement of dengue virus infection in U937 cells requires cholesterol-rich membrane microdomains

1 Departamento de Infectómica y Patogénesis Molecular, CINVESTAV-IPN, Mexico, DF, Mexico 2 Centro de Microbiología y Biología Celular, IVIC, Caracas, Venezuela Correspondence Rosa María del Angel rmangel{at}cinvestav.mx Dengue virus (DENV) is the causative agent of dengue fever and the more severe f...

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Published in:Journal of general virology 2010-02, Vol.91 (2), p.394-403
Main Authors: Puerta-Guardo, Henry, Mosso, Clemente, Medina, Fernando, Liprandi, Ferdinando, Ludert, Juan E, del Angel, Rosa Maria
Format: Article
Language:English
Subjects:
Antibody-Dependent Enhancement
Biological and medical sciences
Cholesterol - metabolism
Dengue virus
Dengue Virus - physiology
Fundamental and applied biological sciences. Psychology
Humans
Membrane Microdomains - metabolism
Membrane Microdomains - virology
Microbiology
Miscellaneous
Severe Dengue - metabolism
Severe Dengue - virology
U937 Cells
Virology
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Summary:1 Departamento de Infectómica y Patogénesis Molecular, CINVESTAV-IPN, Mexico, DF, Mexico 2 Centro de Microbiología y Biología Celular, IVIC, Caracas, Venezuela Correspondence Rosa María del Angel rmangel{at}cinvestav.mx Dengue virus (DENV) is the causative agent of dengue fever and the more severe forms of the infection known as dengue haemorrhagic fever and dengue shock syndrome (DHF/DSS). Secondary infections with a serotype different from the primary infection are considered a risk factor for the development of DHF/DSS. One explanation for the increased risk of DHF/DSS development after heterologous secondary infections is the antibody-dependent enhancement (ADE) hypothesis. This hypothesis postulates that pre-existing non-neutralizing antibodies will form immune complexes with the new serotype-infecting virus that in turn will have enhanced capacity to infect macrophages and other Fc receptor (Fc R)-bearing cells. Despite the evidence supporting the ADE hypothesis, the molecular mechanisms of ADE are not fully understood. In this work, we present evidence which indicates that intact lipid rafts are required for the ADE infection of U937 cells with DENV. Flow cytometry analysis to measure the percentage of infected cells showed that treatment of differentiated U937 cells with nystatin (30 µg ml –1 ), filipin (10 µg ml –1 ) or β -methyl cyclodextrin (30 mM) significantly reduces ( P
ISSN:0022-1317
1465-2099
DOI:10.1099/vir.0.015420-0