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Journal of Virology, January 2001, p. 1077-1082, Vol. 75, No. 2
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.2.1077-1082.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

LFA-1 Expression on Target Cells Promotes Human Immunodeficiency Virus Type 1 Infection and Transmission

Catarina E. Hioe,1,* Peter C. Chien Jr.,1 ChaFen Lu,2 Timothy A. Springer,2 Xiao-Hong Wang,1 Juan Bandres,1 and Michael Tuen1

New York University School of Medicine and Manhattan VA Medical Center, New York, New York 10010,1 and The Center for Blood Research and Harvard Medical School, Boston, Massachusetts 021152

Received 26 May 2000/Accepted 25 October 2000

While CD4 and the chemokine receptors are the principal receptors for human immunodeficiency virus (HIV), other cellular proteins, such as LFA-1, are also involved in HIV infection. LFA-1 and its ligands, ICAM-1, ICAM-2, and ICAM-3, can be expressed on the cells infected by HIV, as well as on the HIV virions themselves. To examine the role of LFA-1 expressed on target cells in HIV infection, Jurkat-derived Jbeta 2.7 T-cell lines that express either wild-type LFA-1, a constitutively active mutant LFA-1, or no LFA-1 were used. The presence of wild-type LFA-1 enhanced the initial processes of HIV infection, as well as the subsequent replication and transmission from cell to cell. In contrast, the constitutively active LFA-1 mutant failed to promote virus replication and spread, even though this mutant could help HIV enter cells and establish the initial infection. This study clearly demonstrates the contribution of LFA-1 in the different stages of HIV infection. Moreover, not only is LFA-1 expression important for initial HIV-cell interaction, subsequent replication, and transmission, but its activity must also be properly regulated.


* Corresponding author. Mailing address: VA Medical Center---Research Service, 423 E. 23rd St., Room 18-124 North, New York, NY 10010. Phone: (212) 263-6769. Fax: (212) 951-6321. E-mail: hioec01{at}med.nyu.edu.


Journal of Virology, January 2001, p. 1077-1082, Vol. 75, No. 2
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.2.1077-1082.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



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