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Blood, 23 April 2009, Vol. 113, No. 17, pp. 4086-4093. Prepublished online as a Blood First Edition Paper on November 20, 2008; DOI 10.1182/blood-2008-09-181073. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-09-181073v1 113/17/4086    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Zhang, W. Articles by Karpatkin, S. Search for Related Content PubMed PubMed Citation Articles by Zhang, W. Articles by Karpatkin, S. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLATELETS AND THROMBOPOIESIS Role of molecular mimicry of hepatitis C virus protein with platelet GPIIIa in hepatitis C–related immunologic thrombocytopenia Wei Zhang1, Michael A. Nardi2, William Borkowsky2, Zongdong Li1, and Simon Karpatkin1 Departments of 1 Medicine and 2 Pediatrics, New York University School of Medicine, NY Patients with HIV-1 immune-related thrombocytopenia (HIV-1–ITP) have a unique Ab against platelet GPIIIa49-66 capable of inducing oxidative platelet fragmentation in the absence of complement. HIV-1–seropositive drug abusers are more prone to develop immune thrombocytopenia than non–drug abusers and have a higher coinfection with hepatitis C virus (HCV) than non–drug abusers (90% vs 30%). Molecular mimicry was sought by screening a phage peptide library with anti–GPIIIa49-66 antibody as bait for peptides sharing homology sequences with HCV. Several phage peptide clones had 70% homology with HCV protein. Sera from dually infected thrombocytopenic patients with HCV and HIV-ITP reacted strongly with 4 nonconserved peptides from HCV core envelope 1. Reactivity correlated inversely with platelet count (r2 = 0.7, P < .01). Ab raised against peptide PHC09 in GPIIIa–/– mice induced thrombocytopenia in wild-type mice. Affinity-purified IgG against PHC09 induced oxidative platelet fragmentation in vitro. Drug abusers dually infected with HCV and HIV-1 had a greater incidence and severity of thrombocytopenia as well as titer of anti–GPIIIa49-66/PHC09 Ab. NZB/W F1 mice injected with recombinant core envelope 1 developed Ab versus PHC09 and significantly decreased their platelet count (P < .001). Thus, HCV core envelope 1 can induce thrombocytopenia by molecular mimicry with GPIIIa49-66. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Molecular mimicry and immune thrombocytopenia Richard H. Aster Blood 2009 113: 3887-3888. [Full Text] [PDF] This article has been cited by other articles: D. B. Cines, J. B. Bussel, H. A. Liebman, and E. T. Luning Prak The ITP syndrome: pathogenic and clinical diversity Blood, June 25, 2009; 113(26): 6511 - 6521. [Abstract] [Full Text] [PDF] Z. Li, M. A. Nardi, Y.-S. Li, W. Zhang, R. Pan, S. Dang, H. Yee, D. Quartermain, S. Jonas, and S. Karpatkin C-terminal ADAMTS-18 fragment induces oxidative platelet fragmentation, dissolves platelet aggregates, and protects against carotid artery occlusion and cerebral stroke Blood, June 11, 2009; 113(24): 6051 - 6060. [Abstract] [Full Text] [PDF] R. H. Aster Molecular mimicry and immune thrombocytopenia Blood, April 23, 2009; 113(17): 3887 - 3888. [Full Text] [PDF]

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