Final answer:
Individuals carrying the CCR5-Δ32 allele exhibit resistance to HIV by lacking the functional CCR5 co-receptor needed for some strains of the virus to enter T-cells. Those homozygous for the allele have great resistance, while heterozygous individuals have partial protection. This discovery has informed HIV research, including drug development targeting CCR5 binding inhibition.
Step-by-step explanation:
Individuals with the CCR5-Δ32 allele exhibit a compelling phenotype: resistance to HIV infection. The CCR5 protein is a receptor on the surface of T-cells that HIV usually uses to enter and infect the cell. However, people possessing two copies of the CCR5-Δ32 allele (homozygous) lack the functional receptor that certain strains of HIV require to bind and enter cells, granting them a heightened resistance to those strains of HIV. Meanwhile, individuals with one copy of the mutation (heterozygous) also exhibit some level of protection against HIV infection.
The CCR5-Δ32 mutation affects the viral life cycle by inhibiting the virus's ability to bind to the CCR5 co-receptor on the surface of the T-cell, thereby blocking HIV entry. By preventing this critical step of the life cycle, the mutation effectively disarms the virus and forms the basis for ongoing research into HIV therapies, including drugs designed to mimic the mutation's effect by blocking CCR5 binding.
The discovery that the CCR5-Δ32 mutation provides resistance to HIV and the ongoing research on the mutation's prevalence in European populations also underscore an interdisciplinary challenge which brings together genetics, history, and epidemiology to better understand the evolution of human populations and their responses to pandemics like HIV and the Black Death.