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Prepublished online as a Blood First Edition Paper on June 12, 2003; DOI 10.1182/blood-2002-10-3275. This Article Full Text (PDF) All Versions of this Article: 2002-10-3275v1 102/7/2334    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Fantuzzi, L. Articles by Gessani, S. Search for Related Content PubMed PubMed Citation Articles by Fantuzzi, L. Articles by Gessani, S. Social Bookmarking                   What's this? Submitted October 31, 2002 Accepted June 3, 2003 Endogenous CCL2 (monocyte chemotactic protein-1) modulates human immunodeficiency virus type-1 replication and affects cytoskeleton organization in human monocyte-derived macrophages Laura Fantuzzi, Francesca Spadaro, Giuliana Vallanti, Irene Canini, Carlo Ramoni, Elisa Vicenzi, Filippo Belardelli, Guido Poli, and Sandra Gessani* Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy Laboratory of Immunology, Istituto Superiore di Sanita', Rome, Italy AIDS Immunopathogenesis Unit, Department of Immunology and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy AIDS Immunopathogenesis Unit, Department of Immunology and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy; School of Medicine, Vita-Salute University, Milan, Italy * Corresponding author; email: gessani{at}iss.it. CCL2 is constitutively expressed at high levels in human peripheral blood monocytes and its expression is further up-modulated during their differentiation into macrophages as well as in the course of HIV infection. To investigate the role of endogenous CCL2 on HIV replication and macrophage function, its activity was neutralized by specific antibodies. Infection of monocyte-derived macrophages with laboratory-adapted HIV-1 or primary viral isolates in the continuous presence of anti-CCL2 antibody resulted in significantly lower p24 Gag antigen release with respect to control cultures. Interestingly, CCL2 neutralization did not affect the early steps of the HIV life cycle but resulted in the intracellular accumulation of p24 Gag antigen. Simultaneously, remarkable changes in cell morphology and size occurred in cell cultures maintained in the presence of anti-CCL2 antibody. 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