Journal
JOURNAL OF VIROLOGY
Volume 75, Issue 2, Pages 1077-1082Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.75.2.1077-1082.2001
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Funding
- NHLBI NIH HHS [HL59725, R01 HL059725] Funding Source: Medline
- NIAID NIH HHS [AI32424] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL059725] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI032424] Funding Source: NIH RePORTER
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While CD4 and the chemokine receptors are the principal receptors for human immunodeficiency virus (HN), other cellular proteins, such as LFA-1, are also involved in HIV infection. LFA-1 end 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 J beta2.7 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-T in the different stages of HIV infection. Moreover, not only is LFA-1 expression important for initial HN-cell interaction, subsequent replication, and transmission, but its activity must also be properly regulated.
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