the infection of cells by the human immunodeficiency virus (hiv) requires the virus to bind to the cell surface molecule cd3 and a second coreceptor molecule, ccr5 or cxcr4. in scandinavian populations a mutation in ccr5 results in functional loss of ccr5 expression and exists at an allelic frequency of about 10 to 18 percent. homozygous loss-of-function carriers are protected from infection by hiv strains that bind ccr5, and this mutation is also believed to have been protective against smallpox infection. this ccr5 mutation is evidence that mutations

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The two kinds of HIV resistance that exist are caused by a genetic variation called CCR5-delta 32. HIV is prevented from entering immune cells by CCR5-delta 32.

The CCR5 co-receptor on cells' exteriors shrinks more than usual and stops sticking out from the cell as a result of the mutation. The CCR5 co-receptor functions as a doorway for HIV to enter cells. In a sense, the CCR5-delta 32 mutation "locks the door," preventing HIV from entering the cell. 1% of Northern European descendants, especially Swedes, are immune to HIV infection. These fortunate individuals are homozygous carriers of the mutant gene, which means they received a copy from each parent.One copy of the gene was inherited by an additional 10–15% (some sources put the percentage as high as 18%) of people of European ancestry. A mutation with only one copy does not protect against infection. But it does slow the spread of AIDS and lessen the risk of infection for the carrier. The CCR5-delta 32 mutation has not been identified in Africans, East Asians, or Amerindians because it is primarily associated with the Eurasia region.

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