Genetic mutations are not uncommon. They can happen for a variety of reasons and have a variety of effects. Those with negative effects are weeded out by natural selection, and those with positive effects prevail and are accumulated due to natural selection. These mutations can be caused by a variety of reasons such as copying errors during cell division, exposure to ultraviolet rays and viruses, or can happen deliberately (Wikipedia). Most mutations have no effect on a species or its individuals because DNA repair is quite successful in fixing most mistakes before they become permanent. But there are very few mutations which have beneficial consequences. One such mutation that results in benefits for a species/individuals that make it up, is the CCR5-Delta32 mutation. During this mutation the Delta32 base pair is deleted in human CCR5 which results in immunity to HIV Type 1 (if homozygous) or increased resistance to AIDS (if heterozygous) (Wikipedia). The very controversial current argument on this subject asks several questions: if the absence of the CCR5-Delta32 is ultimately beneficial to humans, or if its negative side effects outweigh the benefits; as well as, where the origins of this mutation are.
[...] The CCR5-Delta 32 Genetic Mutation and Human Evolution Genetic mutations are not uncommon. They can happen for a variety of reasons and have a variety of effects. Those with negative effects are weeded out by natural selection, and those with positive effects prevail and are accumulated due to natural selection. These mutations can be caused by a variety of reasons such as copying errors during cell division, exposure to ultraviolet rays and viruses, or can happen deliberately (Wikipedia). Most mutations have no effect on a species or its individuals because DNA repair is quite successful in fixing most mistakes before they become permanent. [...]
[...] There is also another possibility that this mutation is much older and has resulted due to smallpox outbreaks in Europe, which is the less popular theory. Some would argue that CCR5-Delta32 allele is under high selective pressure at the moment in populations with high incidence of HIV-1, yet HIV- 1 does not have a long history of affecting humans which would make it unaccountable for the “selective rise of this resistance allele” (Kampis). This it the reason why some scientists argue that its origins are in smallpox due to the continuous mortality (due to smallpox) throughout history, as well as the fact that it is transmitted between humans and does not involve rodents or fleas. [...]
[...] “CCR5 Delta 32 protein expression and stability are critical for resistance to human immunodeficiency virus type 1 in vivo.” Journal of Virology. August 2007. Vol Number 15, pages 8041- Becker, Yechiel. Molecular Mechanism of Human Resistance to HIV-1 Infection in Persistently Infected Individuals—A Review, Hypothesis and Implications.” Virus Genes. August 2005. Volume 31, Number 1. pages 112- Wikipedia Encyclopedia, www.wikipedia.org 4. Delfraissy, J.F.; Laurichesse, J.J.; Meyer, L.; Persoz, A.; Theodorou, I.; Rouzioux, C . “Improved virological response to highly active antiretroviral therapy in HIV-1- infected patients carrying the [...]
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