There’s compelling evidence that certain immunity to HIV may be linked to a genetic mutation known as CCR5-Δ32. This mutation likely emerged in response to historical plagues, possibly the bubonic plague or smallpox. This mutation involves a deletion in the CCR5 gene. This gene codes for a receptor on the surface of white blood cells. HIV uses this receptor to enter and infect cells. People with two copies of this mutation, one from each parent, are highly resistant to HIV infection. The virus cannot enter their cells.
Here’s how it connects to ancient plagues:
- High Frequency in Europe: The CCR5-Δ32 mutation is notably common among people of European descent, where it appears in about 10% of the population. It’s much rarer or nearly absent in other populations, which aligns with the geographic impact of historic plagues in Europe, especially the bubonic plague and smallpox, both of which ravaged Europe for centuries.
- Selective Pressure from Historical Pandemics: The high prevalence of CCR5-Δ32 in Europe suggests it was positively selected. Researchers theorize that during the bubonic plague or smallpox epidemics, individuals with this mutation had a survival advantage, as these diseases may have also used the CCR5 receptor pathway.
- Protection Against HIV: The mutation’s relevance to HIV immunity was discovered later. People with two copies of CCR5-Δ32 are almost entirely immune to HIV infection, while those with one copy may have a delayed progression if infected. This suggests that the mutation, originally advantageous against historic pathogens, inadvertently protects against HIV.
While it’s uncertain if CCR5-Δ32 specifically evolved in response to the bubonic plague or other pandemics, it’s clear that the mutation has roots in an ancestral selection pressure, likely due to a severe, recurrent epidemic.
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