How HIV uses CCR5 to get inside
HIV cannot simply pass through an immune cell’s outer membrane. To infect many of the immune cells it targets, the virus first attaches to the CD4 protein on the cell surface, then uses a second protein—often CCR5—as a co-receptor, or entry point. Once the virus docks with both, it can fuse with the cell and deliver its genetic material inside.
CCR5-Δ32 is a deletion in the gene that makes the CCR5 protein. In people who inherit two copies, cells generally display little or no working CCR5 on their surfaces. Without that co-receptor, HIV strains that depend on CCR5 have trouble entering those cells and establishing infection.
Protection depends on the virus—and the inheritance
The mutation is not a general-purpose shield. Some HIV strains use a different co-receptor, called CXCR4, and can infect cells without CCR5. Having one copy of CCR5-Δ32 can also reduce the amount of working CCR5 without eliminating it, so the effect is not the same as having two copies.
That distinction helps explain why CCR5-Δ32 is important in HIV research: it identifies a specific step in infection that can sometimes be blocked. It does not make the immune system invulnerable. The protection is tied to whether a virus relies on CCR5—and to how much functional CCR5 a person’s cells still make.
