Final answer:
The CCR5-Δ32 mutation results in HIV resistance by preventing viral entry into T cells, with homozygous individuals having a high resistance and heterozygous individuals having some protection. The mutation's historical selective advantage, possibly due to past epidemics, is still debated among researchers.
Step-by-step explanation:
The variation of the CCR5 coreceptor in question is the CCR5-Δ32 mutation, which provides resistance against HIV infection. This mutation leads to the production of a CCR5 receptor that HIV cannot effectively bind to, thus blocking the virus's entry into host T cells. Having two copies of this mutation (homozygous) provides a strong resistance, while having one copy (heterozygous) offers some protection.
The role that this mutation plays in the inhibition of the virus life cycle is during the entry phase, where HIV typically uses CD4 and a co-receptor like CCR5 or CXCR4 to enter a cell. The absence of a functional CCR5 prevents the virus from entering the cell and starting the infection process.
Debate has surrounded the origin and selective advantage of the CCR5-Δ32 mutation. While past epidemics such as the plague have been suggested as a selective force, these theories have not been conclusively proven, and the discussion intersects the fields of genetics, immunology, and history.