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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3449-3456. Prepublished online as a Blood First Edition Paper on August 2, 2005; DOI 10.1182/blood-2005-02-0536. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-02-0536v1 106/10/3449    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 Munakata, Y. Articles by Sasaki, T. Search for Related Content PubMed PubMed Citation Articles by Munakata, Y. Articles by Sasaki, T. Related Collections Hematopoiesis Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Ku80 autoantigen as a cellular coreceptor for human parvovirus B19 infection Yasuhiko Munakata, Takako Saito-Ito, Keiko Kumura-Ishii, Jie Huang, Takao Kodera, Tomonori Ishii, Yasuhiko Hirabayashi, Yoshio Koyanagi, and Takeshi Sasaki From the Department of Rheumatology and Hematology, and Department of Virology, Tohoku University Graduate School of Medicine, Sendai, Japan. Human parvovirus B19 (B19) infects human erythroid cells expressing P antigen. However, some cell lines that were positive for P antigen failed to bind B19, whereas some cell lines had an ability to bind B19 despite undetectable expression of P antigen. We here demonstrate that B19 specifically binds with Ku80 autoantigen on the cell surface. Furthermore, transfection of HeLa cells with the gene of Ku80 enabled the binding of B19 and allowed its entry into cells. Moreover, reduction of cell-surface expression of Ku80 in KU812Ep6 cells, which was a high-sensitive cell line for B19 infection, by short interfering RNA for Ku80 resulted in the marked inhibition of B19 binding in KU812Ep6 cells. Although Ku80 originally has been described as a nuclear protein, human bone marrow erythroid cells with glycophorin A or CD36, B cells with CD20, or T cells with CD3 were all positive for cell-surface expression of Ku80. B19 infection of KU812Ep6 cells and bone marrow cells was inhibited in the presence of anti-Ku80 antibody. Our data suggest that Ku80 functions as a novel coreceptor for B19 infection, and this finding may provide an explanation for the pathologic immunity associated with B19 infection. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Wong, N. Zhi, C. Filippone, K. Keyvanfar, S. Kajigaya, K. E. Brown, and N. S. Young Ex Vivo-Generated CD36+ Erythroid Progenitors Are Highly Permissive to Human Parvovirus B19 Replication J. Virol., March 1, 2008; 82(5): 2470 - 2476. [Abstract] [Full Text] [PDF] M. Waldman and J. B. Kopp Parvovirus B19 and the Kidney Clin. J. Am. Soc. Nephrol., July 1, 2007; 2(Supplement_1): S47 - S56. [Abstract] [Full Text] [PDF] A. Lupescu, C.-T. Bock, P. A. Lang, S. Aberle, H. Kaiser, R. Kandolf, and F. Lang Phospholipase A2 Activity-Dependent Stimulation of Ca2+ Entry by Human Parvovirus B19 Capsid Protein VP1 J. Virol., November 15, 2006; 80(22): 11370 - 11380. [Abstract] [Full Text] [PDF]

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