Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 24, Pages 13916-13921Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01585-07
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Funding
- Medical Research Council [G0400453] Funding Source: Medline
- MRC [G0400453] Funding Source: UKRI
- Medical Research Council [G0400453] Funding Source: researchfish
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Human immunodeficiency virus type 1 (HIV-1) can spread between CD4(+) T cells by using a virological synapse (VS). The VS assembly is a cytoskeleton-driven process dependent on HIV-1 envelope glycoprotein (Env)-receptor engagement and is hypothesized to require adhesion molecule interactions. Here we demonstrate that leukocyte function-associated antigen 1 (LFA-1), intercellular adhesion molecule 1 (ICAM-1), and ICAM-3 are enriched at the VS and that inhibition of these interactions influences conjugate formation and reduces VS assembly. Moreover, CD4(+) T cells deficient in LFA-1 or with modified LFA-1 function were less able to support VS assembly and cell-cell transfer of HIV-1. Thus, cognate adhesion molecule interactions at the VS are important for HIV-1 spread between T cells.
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