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 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 Gabali, A. M.
Right arrow Articles by Thomas, L. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gabali, A. M.
Right arrow Articles by Thomas, L. L.

 Previous Article  |  Next Article 

Journal of Virology, October 2004, p. 10833-10836, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10833-10836.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Activation by Inflammatory Stimuli Increases Neutrophil Binding of Human Immunodeficiency Virus Type 1 and Subsequent Infection of Lymphocytes

Ali M. Gabali, Joshua J. Anzinger, Gregory T. Spear, and Larry L. Thomas*

Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois

Received 4 February 2004/ Accepted 18 May 2004

Resting neutrophils bind human immunodeficiency virus type 1 (HIV-1) and efficiently transfer infection to lymphocytes. The present study shows that a brief activation by inflammatory stimuli increases the neutrophil binding levels of both R5 and X4 isolates of HIV-1 at least twofold. The binding occurs independently of CD4, gp120, and incubation temperature and is observed with HIV-1 propagated either in lymphocytes or in HEK293 cells. Significantly, HIV-1 bound to the activated neutrophils accelerates the infection of activated lymphocytes compared to free HIV-1 or to HIV-1 bound to resting neutrophils. It is proposed that these events may contribute to the increased risk of HIV-1 transmission at sites of mucosal infection.


* Corresponding author. Mailing address: Department of Immunology/Microbiology, Rush University Medical Center, 1653 W. Congress Pkwy., Chicago, IL 60612. Phone: (312) 942-3518. Fax: (312) 942-2808. E-mail: lthomas2{at}rush.edu.


Journal of Virology, October 2004, p. 10833-10836, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10833-10836.2004
Copyright © 2004, 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 © 2004 by the American Society for Microbiology. All rights reserved.