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...mutation are highly resistant to HIV-1 infection (Samson et al. 1996; Dean et al. 1996; Libert et al. 1998), whereas heterozygotes have slower rate of progression to disease (Grimaldi et al. 2002; Samson et al. 1996; Dean et al. 1996). The CCR5-[DELTA]32 mutation also seems to confer protection against several diseases, namely, arterial occlusive disease (Ghilardi et al. 2004), rheumatoid arthritis (Pokorny et al. 2005), breast cancer (Degerli et al. 2005), and hepatitis C virus (Wald et al. 2004).
The CCR5-[DELTA]32 mutation seems to have had its origin in northern Europe, but there is no agreement about its age, which varies from about 700 years ago (with a range of 275-1,875 years) (Stephens et al. 1998) to 5,075 years ago (with a range of 3,150 to 7,800 years) (Sabeti et al. 2005). Lucotte (2001) put forward the hypothesis of a Viking origin for the mutation, suggesting that the mutation already existed in Scandinavia before the Vikings dispersed 1,000-1,200 years ago. A study in Europe shows a high frequency of the CCR5-[DELTA]32 mutation in areas usually associated with Viking culture, namely, Iceland (14.7%) and Sweden (14.2%) (Lucotte 2001), with decreasing frequencies running toward southern Europe (Libert et al. 1998). A study of sub-Saharan Africans shows a very low frequency (0.16%) of the mutation for this region (Lucotte 1997), and for North Africa the values are lower ([approximately equal to] 1.5%) than those in Southern Europe (Lucotte 2001), suggesting a European influence in North Africa.
In Europe the gene frequency of the CCR5-[DELTA]32 mutation is about 10%, resulting in a heterozygous frequency of 18% and a homozygous frequency of 1% (Martinson et al. 1997). The mutation's relatively high frequency in Europe has been explained by positive selection of this mutation in those affected by bubonic plague (Stephens et al. 1998), but Galvani and Slatkin (2003) demonstrated that smallpox is a better candidate for positive selection for the CCR5-[DELTA]32 mutation, thus explaining the...
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