This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
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 Google Scholar
Google Scholar
Right arrow Articles by Khurana, S.
Right arrow Articles by Thali, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khurana, S.
Right arrow Articles by Thali, M.

 Previous Article  |  Next Article 

Journal of Virology, November 2007, p. 12630-12640, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01255-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 and Influenza Virus Exit via Different Membrane Microdomains{triangledown} ,{dagger}

Sandhya Khurana,1,2,{ddagger} Dimitry N. Krementsov,1,3,{ddagger} Aymeric de Parseval,4 John H. Elder,4 Michelangelo Foti,5 and Markus Thali1,2,3*

Department of Microbiology and Molecular Genetics,1 Graduate Programs in Microbiology and Molecular Genetics,2 Cellular and Molecular Biology, University of Vermont, Burlington, Vermont 05405,3 Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037,4 Department of Cellular Physiology & Metabolism, University of Geneva, CH-1211 Geneva, Switzerland5

Received 8 June 2007/ Accepted 30 August 2007

Directed release of human immunodeficiency virus type 1 (HIV-1) into the cleft of the virological synapse that can form between infected and uninfected T cells, for example, in lymph nodes, is thought to contribute to the systemic spread of this virus. In contrast, influenza virus, which causes local infections, is shed into the airways of the respiratory tract from free surfaces of epithelial cells. We now demonstrate that such differential release of HIV-1 and influenza virus is paralleled, at the subcellular level, by viral assembly at different microsegments of the plasma membrane of HeLa cells. HIV-1, but not influenza virus, buds through microdomains containing the tetraspanins CD9 and CD63. Consequently, the anti-CD9 antibody K41, which redistributes its antigen and also other tetraspanins to cell-cell adhesion sites, interferes with HIV-1 but not with influenza virus release. Altogether, these data strongly suggest that the bimodal egress of these two pathogenic viruses, like their entry into target cells, is guided by specific sets of host cell proteins.

* Corresponding author. Mailing address: 318 Stafford Hall, University of Vermont, Burlington, VT 05405. Phone: (802) 656-1056. Fax: (802) 656-4789. E-mail: markus.thali{at}uvm.edu

{triangledown} Published ahead of print on 12 September 2007.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} S.K. and D.N.K. contributed equally to this work.

Journal of Virology, November 2007, p. 12630-12640, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01255-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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