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Prepublished online as a Blood First Edition Paper on August 7, 2003; DOI 10.1182/blood-2003-05-1522. This Article Full Text (PDF) All Versions of this Article: 2003-05-1522v1 102/12/3927    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 Weigel-Kelley, K. A Articles by Srivastava, A. Search for Related Content PubMed PubMed Citation Articles by Weigel-Kelley, K. A Articles by Srivastava, A. Social Bookmarking                   What's this? Submitted May 14, 2003 Accepted August 1, 2003 51 integrin as a cellular co-receptor for human parvovirus B19: requirement of functional activation of 1 integrin for viral entry Kirsten A Weigel-Kelley, Mervin C Yoder, and Arun Srivastava* Department of Microbiogy & Immunology, Walther Oncology Center, Walther Cancer Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Division of Hematology/Oncology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA Departments of Pediatrics and Biochemistry & Molecular Biology, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA * Corresponding author; email: asrivast{at}iupui.edu. Replication of the pathogenic human parvovirus B19 is restricted to erythroid progenitor cells. Although blood group P antigen has been reported to be the cell surface receptor for parvovirus B19, a number of non-erythroid cells, which express P antigen, are not permissive for parvovirus B19 infection. We have documented that P antigen is necessary for parvovirus B19 binding, but not sufficient for virus entry into cells. To test whether parvovirus B19 utilizes a cell surface co-receptor for entry, we used human erythroleukemia cells (K562), which allow parvovirus B19 binding, but not entry. We report here that upon treatment with phorbol esters, K562 cells become adherent and permissive for parvovirus B19 entry, which is mediated by 51 integrins, but only in their high affinity conformation. Mature human red blood cells (RBCs), which express high levels of P antigen, but not 51 integrins, bind parvovirus B19, but do not allow viral entry. In contrast, primary human erythroid progenitor cells express high levels of both P antigen and 51 integrins, and allow 1 integrin-mediated entry of parvovirus B19. Thus, in a natural course of infection, RBCs are likely exploited for a highly efficient systemic dissemination of parvovirus B19. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W. Guan, S. Wong, N. Zhi, and J. Qiu The Genome of Human Parvovirus B19 Can Replicate in Nonpermissive Cells with the Help of Adenovirus Genes and Produces Infectious Virus J. Virol., September 15, 2009; 83(18): 9541 - 9553. [Abstract] [Full Text] [PDF] F. Bonvicini, C. Filippone, E. Manaresi, M. Zerbini, M. Musiani, and G. Gallinella HepG2 hepatocellular carcinoma cells are a non-permissive system for B19 virus infection J. Gen. Virol., December 1, 2008; 89(12): 3034 - 3038. [Abstract] [Full Text] [PDF] C. Bonsch, C. Kempf, and C. 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