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Galectin-1 promotes HIV-1 infectivity in macrophages through stabilization of viral adsorption.

Abstract
Following primary infection with human immunodeficiency virus type-1 (HIV-1), macrophages are thought to play an important role, as they are one of the first target cells the virus encounters and can also sustain a significant production of viruses over extended periods of time. While the interaction between the primary cellular receptor CD4 and the virus-encoded external envelope glycoprotein gp120 initiates the infection process, it has been suggested that various host factors are exploited by HIV-1 to facilitate adsorption onto the cell surface. Macrophages and other cells found at the infection site can secrete a soluble mammalian lectin, galectin-1, which binds to beta-galactoside residues through its carbohydrate recognition domain. Being a dimer, galectin-1 can cross-link ligands expressed on different constituents to mediate adhesion between cells or between cells and pathogens. We report here that galectin-1, but not galectin-3, increased HIV-1 infectivity in monocyte-derived macrophages (MDMs). This phenomenon was likely due to an enhancement of virus adsorption kinetics, which facilitates HIV-1 entry. The fusion inhibitors T-20 and TAK779 remained effective at reducing infection even in the presence of galectin-1, indicating that the galectin-1-mediated effect is occurring at a step prior to fusion. Together, our data suggest that galectin-1 can facilitate HIV-1 infection in MDMs by promoting early events of the virus replicative cycle (i.e. adsorption).
AuthorsSimon Mercier, Christian St-Pierre, Isabelle Pelletier, Michel Ouellet, Michel J Tremblay, Sachiko Sato
JournalVirology (Virology) Vol. 371 Issue 1 Pg. 121-9 (Feb 05 2008) ISSN: 0042-6822 [Print] United States
PMID18028978 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Galectin 1
  • Recombinant Proteins
Topics
  • Cell Differentiation
  • Galectin 1 (genetics, metabolism, physiology)
  • HIV Infections (etiology)
  • HIV-1 (pathogenicity)
  • Humans
  • Kinetics
  • Macrophages (virology)
  • Monocytes (cytology)
  • Recombinant Proteins (metabolism)
  • Viruses (metabolism)

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