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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2790-2797. Prepublished online as a Blood First Edition Paper on June 23, 2005; DOI 10.1182/blood-2005-04-1390. This Article Full Text (PDF) All Versions of this Article: 2005-04-1390v1 106/8/2790    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 Caselli, E. Articles by Di Luca, D. Search for Related Content PubMed PubMed Citation Articles by Caselli, E. Articles by Di Luca, D. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 5, 2005 Accepted June 12, 2005 Human herpesvirus 8 enhances human immunodeficiency virus replication in acutely infected cells and induces reactivation in latently infected cells Elisabetta Caselli, Monica Galvan, Enzo Cassai, Arnaldo Caruso, Laura Sighinolfi, and Dario Di Luca* Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Ferrara, Italy Chair of Microbiology, University of Brescia, Brescia, Italy Division of Infectious Diseases, S. Anna Hospital, Ferrara, Italy * Corresponding author; email: ddl{at}unife.it. Human herpesvirus-8 (HHV-8) is etiologically associated with Kaposi's sarcoma (KS), the most common AIDS-associated malignancy. Previous results indicate that the HHV-8 viral transactivator ORF50 interacts synergistically with Tat protein in the transactivation of Human Immunodeficiency Virus (HIV) LTR, leading to increased cell susceptibility to HIV infection. Here, we analyze the effect of HHV-8 infection upon HIV replication in monocyte-macrophage and endothelial cells, as potential targets of coinfection. Primary or transformed monocytic and endothelial cells were infected with a cell free HHV-8 inoculum and subsequently infected with lymphotropic or monocytotropic strains of HIV. The results show that HHV-8 coinfection markedly increases HIV replication in both cell types. HHV-8 infection induces also HIV reactivation in chronically infected cell lines and in PBMCs from asymptomatic HIV patients, suggesting the possibility that similar interactions might take place also in vivo. Furthermore, coinfection is not an essential condition, since contiguity of differently infected cells is sufficient for HIV reactivation. The results suggest that HHV-8 might be a cofactor for HIV progression and that HHV-8 infected endothelial cells might play a relevant role in transendothelial HIV spread. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. West and B. Damania Upregulation of the TLR3 Pathway by Kaposi's Sarcoma-Associated Herpesvirus during Primary Infection J. Virol., June 1, 2008; 82(11): 5440 - 5449. [Abstract] [Full Text] [PDF] V. Fonsato, S. Buttiglieri, M. Chiara Deregibus, B. Bussolati, E. Caselli, D. Di Luca, and G. Camussi PAX2 expression by HHV-8-infected endothelial cells induced a proangiogenic and proinvasive phenotype Blood, March 1, 2008; 111(5): 2806 - 2815. [Abstract] [Full Text] [PDF] E. Caselli, S. Fiorentini, C. Amici, D. Di Luca, A. Caruso, and M. G. Santoro Human herpesvirus 8 acute infection of endothelial cells induces monocyte chemoattractant protein 1-dependent capillary-like structure formation: role of the IKK/NF-{kappa}B pathway Blood, April 1, 2007; 109(7): 2718 - 2726. [Abstract] [Full Text] [PDF]

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