Final answer:
The CCR5Δ5₃₂ mutation hinders the fusion step of the HIV life cycle, blocking the virus from entering the host T-cells. As a result, individuals with this mutation have a natural resistance to HIV-1 infection.
Step-by-step explanation:
People with the CCR5Δ5₃₂ mutation of a T-cell surface protein exhibit resistance to HIV by inhibiting the virus's entry into the host cells. This mutation leads to the production of a malformed CCR5 receptor, which is necessary for HIV-1 to bind and gain entry into T-cells; the virus thus cannot complete its life cycle, particularly the fusion step.
The life cycle of HIV typically involves the following steps: attachment, fusion, reverse transcription, integration, replication, assembly, and budding. The CCR5Δ5₃₂ mutation specifically interferes with the fusion of the HIV-1 virus to the host T-cell. Without the ability to fuse to the host cell membrane, the viral RNA cannot gain entry into the cell, and the subsequent steps in the viral life cycle cannot occur. This mutation thus provides individuals with a natural resistance to HIV-1 infection.
While the CCR5Δ5₃₂ mutation inhibits HIV entry, it is important to note that not all individuals with the mutation are completely immune to HIV-1, and other factors, such as pre-existing immunity and exposure levels, can affect susceptibility. Additionally, different strains of HIV may use alternative co-receptors and are not affected by the CCR5Δ5₃₂ mutation.