Since GBV-C co-infection with HIV initially was associated with a delay in the progression of AIDS in clinical investigations, several mechanisms have been proposed to explain this effect, such as GBV-C infection downregulating HIV entry co-receptors CCR5 and CXCR4 and increasing the secretion of their ligands RANTES, MIP-1α, MIP-1β and SDF-1 [46]. The gene discussed is CCL3; the disease is AIDS.