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Blood, 1 March 2007, Vol. 109, No. 5, pp. 1850-1856. Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2006-07-036046. This Article Full Text Full Text (PDF) Supplemental Methods, Tables, and Figures All Versions of this Article: blood-2006-07-036046v1 109/5/1850    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Pilotti, E. Articles by Casoli, C. Search for Related Content PubMed PubMed Citation Articles by Pilotti, E. Articles by Casoli, C. Related Collections Immunobiology Free Research Articles Chemokines, Cytokines, and Interleukins Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Postgenomic up-regulation of CCL3L1 expression in HTLV-2–infected persons curtails HIV-1 replication Elisabetta Pilotti1, Lisa Elviri2, Elisa Vicenzi3,4, Umberto Bertazzoni5, Maria Carla Re6, Sonia Allibardi7, Guido Poli4,8, and Claudio Casoli1 1 Department of Clinical Medicine, Nephrology, and Health Sciences, University of Parma, Italy; 2 Department of General Chemistry, University of Parma, Italy; 3 Viral Pathogens and Biosafety Unit, San Raffaele Scientific Institute, Milan, Italy; 4 AIDS Immunopathogenesis Unit, San Raffaele Scientific Institute, Milan, Italy; 5 Department of Mother and Child, Biology and Genetic Section, University of Verona, Italy; 6 Department of Clinical and Experimental Medicine, Microbiology Section, University of Bologna, Italy; 7 Human Diagnostics Unit, Celbio, Milan, Italy; 8 Vita-Salute San Raffaele University, School of Medicine, Milan, Italy Leukocytes of persons coinfected with HTLV-2 and HIV-1 secrete chemokines that prevent CCR5-dependent (R5) HIV-1 infection of CD4+ T cells and macrophages, with HTLV-2–induced MIP-1 as dominant HIV-1 inhibitory molecule. Two nonallelic genes code for CCL3 and CCL3L1 isoforms of MIP-1, and the population-specific copy number of CCL3L1 exerts a profound effect on HIV-1 susceptibility and disease progression. Here, we demonstrate that CCL3L1 is secreted spontaneously by leukocytes of HTLV-2–infected persons and superinduced when cells of HTLV-2/HIV-1 multiply exposed-uninfected seronegative (MEU) persons were stimulated with HIV-1 Env peptides. The CCL3L1 median copy number in MEU, HTLV-2/HIV-1–coinfected long-term nonprogressors (LTNPs) and HIV-1–monoinfected LTNPs were 1, 2, and 3, respectively. An increased CCL3L1/CCL3 mRNA ratio versus PHA-activated healthy leukocytes was observed in both HIV-1–monoinfected LTNPs and in HTLV-2/HIV-1MEU subjects. An additional potential correlate of HTLV-2 infection was a rapid and persistent leukocyte secretion of GM-CSF and IFN-, 2 cytokines endowed with CCR5 down-regulation capacity. This study confirms a crucial protective role of CCL3L1 from both HIV infection and disease progression, highlighting a previously not described functional up-regulation of this chemokine variant in both HIV-positive and -negative persons infected with HTLV-2. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: HTLV-IIb reduces HIV infection Davide Zella Blood 2007 109: 1792. [Full Text] [PDF]

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