However, analysis of infection efficiency revealed that the percentage of HIV-p24+ macrophages remained comparable between TAK-779-untreated and treated groups (41.0 ± 14.4% vs. 37.9 ± 14.7% respectively; Figure 3B), suggesting that while CCR5 plays a role in enhancing adhesion, additional mechanisms beyond gp120–CCR5 interaction are involved in mediating viral entry and productive infection in macrophages. This evidence concerns the gene CD9 and infection.