Final Answer:
Individuals who exhibit resistance to developing AIDS once infected by HIV usually possess a genetic mutation that affects the CCR5 receptor.
Step-by-step explanation:
HIV, the human immunodeficiency virus, primarily enters cells by binding to the CD4 receptor and a co-receptor, usually CCR5 or CXCR4, on the surface of immune cells. The CCR5 receptor is crucial for the initial stages of HIV infection. Some individuals carry a genetic mutation known as Δ32 in the CCR5 gene, resulting in a truncated or non-functional CCR5 receptor. This mutation confers resistance to HIV infection and progression to AIDS.
The Δ32 mutation is inherited in an autosomal recessive manner, meaning that individuals need to inherit the mutated gene from both parents to exhibit resistance. Heterozygous individuals (carrying one mutated and one normal allele) may experience slower disease progression. The mutation is more prevalent in populations of European descent, with varying frequencies in different regions.
Studies have shown that individuals with the CCR5 Δ32 mutation are less susceptible to HIV infection and, if infected, progress more slowly to AIDS. This resistance is due to the inability of the virus to utilize the defective CCR5 receptor for cell entry. Understanding the genetic basis of resistance to HIV has important implications for developing therapies and preventive measures in the ongoing battle against the global HIV/AIDS epidemic.