This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Krautkrämer, E.
Right arrow Articles by Zeier, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krautkrämer, E.
Right arrow Articles by Zeier, M.

 Previous Article  |  Next Article 

Journal of Virology, May 2008, p. 4257-4264, Vol. 82, No. 9
0022-538X/08/$08.00+0     doi:10.1128/JVI.02210-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Hantavirus Causing Hemorrhagic Fever with Renal Syndrome Enters from the Apical Surface and Requires Decay-Accelerating Factor (DAF/CD55){triangledown}

Ellen Krautkrämer* and Martin Zeier

Department of Nephrology, University of Heidelberg, Heidelberg, Germany

Received 10 October 2007/ Accepted 17 February 2008

The Old World hantaviruses, members of the family Bunyaviridae, cause hemorrhagic fever with renal syndrome (HFRS). Transmission to humans occurs via inhalation of aerosols contaminated with the excreta of infected rodents. The viral antigen is detectable in dendritic cells, macrophages, lymphocytes, and, most importantly, microvascular endothelial cells. However, the site and detailed mechanism of entry of HFRS-causing hantaviruses in polarized epithelial cells have not yet been defined. Therefore, this study focused on the entry of the pathogenic hantaviruses Hantaan and Puumala into African green monkey kidney epithelial cells and primary human endothelial cells. The polarized epithelial and endothelial cells were found to be susceptible to hantavirus infection exclusively from the apical surface. Treatment with phosphatidylinositol-specific phospholipase C, which removes glycosylphosphatidylinositol (GPI)-anchored proteins from the cell surface, protects cells from infection, indicating that hantaviruses require a GPI-anchored protein as a cofactor for entry. Decay-accelerating factor (DAF)/CD55 is a GPI-anchored protein of the complement regulatory system and serves as a receptor for attachment to the apical cell surface for a number of viruses. Infection was reduced by the pretreatment of hantaviral particles with human recombinant DAF. Moreover, the treatment of permissive cells with DAF-specific antibody blocked infection. These results demonstrate that the Old World hantaviruses Hantaan and Puumala enter polarized target cells from the apical site and that DAF is a critical cofactor for infection.

* Corresponding author. Mailing address: Department of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, D-69120 Heidelberg, Germany. Phone: 49 6221 91120. Fax: 49 6221 9112209. E-mail: ellen_krautkraemer{at}med.uni-heidelberg.de

{triangledown} Published ahead of print on 27 February 2008.

Journal of Virology, May 2008, p. 4257-4264, Vol. 82, No. 9
0022-538X/08/$08.00+0     doi:10.1128/JVI.02210-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Handke, W., Oelschlegel, R., Franke, R., Kruger, D. H., Rang, A. (2009). Hantaan Virus Triggers TLR3-Dependent Innate Immune Responses. J. Immunol. 182: 2849-2858 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»