JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.02070-06v1
81/5/2158    most recent
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 Connolly-Andersen, A.-M.
Right arrow Articles by Mirazimi, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Connolly-Andersen, A.-M.
Right arrow Articles by Mirazimi, A.

 Previous Article  |  Next Article 

Journal of Virology, March 2007, p. 2158-2164, Vol. 81, No. 5
0022-538X/07/$08.00+0     doi:10.1128/JVI.02070-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Basolateral Entry and Release of Crimean-Congo Hemorrhagic Fever Virus in Polarized MDCK-1 Cells{triangledown}

Anne-Marie Connolly-Andersen,1,2 Karl-Erik Magnusson,3 and Ali Mirazimi1,2*

KCB/Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden,1 MTC/Karolinska Institute, SE-171 77 Stockholm, Sweden,2 Division of Medical Microbiology, Faculty of Health Sciences, SE-581 83 Linköping, Sweden3

Received 21 September 2006/ Accepted 1 December 2006

Crimean-Congo hemorrhagic fever virus (CCHFV) is an etiological agent of a disease with mortality rates in patients averaging 30%. The disease is characterized by fever, myalgia, and hemorrhage. Mechanisms underlying the hemorrhage have to our knowledge not been elucidated for CCHFV. Possibly, a direct or indirect viral effect on tight junctions (TJ) could cause the hemorrhage observed in patients, as TJ play a crucial role in vascular homeostasis and can cause leakage upon deregulation. Moreover, there is no knowledge regarding the site of entry and release of CCHFV in polarized epithelial cells. Such cells represent a barrier to virus dissemination within the host, and as a site of viral entry and release, they could play a key role in further spread. For the first time, we have shown preferential basolateral entry of CCHFV in Madin-Darby canine kidney 1 (MDCK-1) epithelial cells. Furthermore, we demonstrated basolateral release of CCHFV in polarized epithelial cells. Interestingly, by measuring transepithelial electrical resistance, we found no effect of CCHFV replication on the function of TJ in this study. Neither did we observe any difference in the localization of the TJ proteins ZO-1 and occludin in CCHFV-infected cells compared to mock-infected cells.

* Corresponding author. Mailing address: Swedish Institute for Infectious Disease Control, Centre for Microbiological Preparedness, SE-171 82 Solna, Sweden. Phone: 46 8 457 25 73. Fax: 46 8 307 957. E-mail: Ali.Mirazimi{at}smi.ki.se.

{triangledown} Published ahead of print on 13 December 2006.

Journal of Virology, March 2007, p. 2158-2164, Vol. 81, No. 5
0022-538X/07/$08.00+0     doi:10.1128/JVI.02070-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2007 by the American Society for Microbiology. All rights reserved.