Recent data suggest that during HIV-1 infection, however, syncytin-1 favors the fusion of HIV-infected T cells and non-infected placental trophoblast cells, hence enhancing viral transmission (36), changing viral tropism toward trophoblast cells (36), and establishing HIV reservoirs in tissues, where antiretroviral therapy (ART) may demonstrate reduced bioavailability (36). The gene discussed is ERVW-1; the disease is HIV-1 infection.