Finally, pretreatment of J-LAT cells with tunicamycin, an inhibitor of the N-glycosylation pathway, markedly reduced binding of Gal-1 (Fig. 4F) and prevented Gal-1-driven latency reversal (Fig. 4G) in J-LAT cells, highlighting the importance of cell surface N-glycans in Gal-1-mediated reactivation of latent HIV-1 infection. This evidence concerns the gene LGALS1 and HIV-1 infection.