Induction of Galectin-1 in HIV- infected CD4+ T cells counteracts viral replication

JULIA RUBIONE; JORGE GEFFNER; GABRIEL RABINOVICH; GABRIEL DUETTE; KARINA MARIÑO; MATÍAS OSTROWSKI; PEHUEN PEREYRA GERBER; MARTA TOSCANO

Simposio; GlycoAr 2016; 2016

The sequential action of glycosyltransferases and glycosidases are responsible for modifying cell surface´s glycans (cellular glycome). These changes can either expose or mask ligands for endogenous lectins, such as Galectins (Gal). Extracellular Gal-1 has important immunomodulatory functions by selectively deleting Th1 and Th17 cells and enabling the expansion of regulatory T cells. Herein, we show that in vitro infection of CD4+ T cells remarkably induces the expression and secretion of Gal-1. Moreover, HIV-infected cells exhibit an increase binding of extracellular Gal-1 to their surface, suggesting that during HIV infection the cellular glycome is modified. Interference RNA-mediated inhibition of Gal-1 expression led to enhanced replication of HIV. These results suggest that by inducing Gal-1 expression, CD4+ T cells autonomously counteract HIV propagation. We are currently characterizing the mechanisms responsible for triggering Gal-1 expression in HIV-infected cells and those involved in inhibiting viral replication.