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This Article Full Text (PDF) 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 Alter, H. J. Search for Related Content PubMed PubMed Citation Articles by Alter, H. J. Social Bookmarking                   What's this? Next Article  Blood, 15 October 2001, Vol. 98, No. 8, pp. 2291-2291 An unexpected link between HCV and platelets Neither the cellular binding sites nor the extrahepatic reservoirs for the hepatitis C virus (HCV) are well understood. The study of Hamaia and colleagues (page 2293) investigates the characteristics of HCV binding to platelets and 2 mononuclear cell lines. Among the interesting findings of this study: (1) Most HCV (95%) circulates bound to IgG; only 1% of circulating virus is cell bound. (2) HCV binds efficiently to platelets. (3) The mechanism of HCV binding to platelets is different than to mononuclear cells in that platelets bind free and complexed HCV equally well and that platelet binding does not reach a saturation limit; platelet binding may represent simple absorption. (4) Although CD81 has been proposed as a major receptor for HCV binding, HCV binds equally to CD81+ cells (MOLT-4) and CD81 cells (U-937 and platelets) and antibody to CD81 does not block HCV binding. Thus, CD81-independent binding sites must exist. (5) The hypervariable region 1 (HVR1) of HCV appears to play an important role in viral attachment. (6) The binding characteristics of recombinant HCV envelope (rE2) are different than those of native HCV, suggesting that studies that employ rE2 may not be fully representative of natural infection. The implications of this study are that platelets as well as mononuclear cells may serve to transport HCV to sites of immune recognition or alternately to sequester virions from such recognition. In addition, these hematologic cells may serve as important reservoirs of HCV that account for the almost universal infection of HCV-naive livers following liver transplantation. This study also indicates that HCV binding is not dependent on the postulated HCV receptor, CD81, and that HVR1 serves as an important attachment site of the virion. HVR1 is also the region presumed to be the target for neutralizing antibody against HCV and the region that under immune pressure mutates to create the vast HCV quasi species. Harvey J. Alter National Institutes of Health CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Leiba, L. Cahalon, A. Shimoni, O. Lider, A. Zanin-Zhorov, I. Hecht, U. Sela, I. Vlodavsky, and A. Nagler Halofuginone inhibits NF-{kappa}B and p38 MAPK in activated T cells J. Leukoc. Biol., August 1, 2006; 80(2): 399 - 406. [Abstract] [Full Text] [PDF] This Article Full Text (PDF) 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 Alter, H. J. Search for Related Content PubMed PubMed Citation Articles by Alter, H. J. Social Bookmarking                   What's this?

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