Editing Mutation (section)

== Beneficial and conditional mutations ==
Although mutations that cause changes in protein sequences can be harmful to an organism, on occasions the effect may be positive in a given environment. In this case, the mutation may enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly. In these cases a mutation will tend to become more common in a population through natural selection. That said, the same mutation can be beneficial in one condition and disadvantageous in another condition. Examples include the following:

'''HIV resistance''': a specific 32 base pair deletion in human [[CCR5]] ([[CCR5#CCR5-Δ32|CCR5-Δ32]]) confers [[HIV]] resistance to [[Zygosity|homozygotes]] and delays [[AIDS]] onset in heterozygotes.<ref>{{cite journal | vauthors = Sullivan AD, Wigginton J, Kirschner D | title = The coreceptor mutation CCR5Delta32 influences the dynamics of HIV epidemics and is selected for by HIV | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 98 | issue = 18 | pages = 10214–9 | date = August 2001 | pmid = 11517319 | pmc = 56941 | doi = 10.1073/pnas.181325198 | bibcode = 2001PNAS...9810214S | doi-access = free }}</ref> One possible explanation of the [[etiology]] of the relatively high frequency of CCR5-Δ32 in the [[Ethnic groups in Europe|European]] population is that it conferred resistance to the [[bubonic plague]] in mid-14th century [[Europe]]. People with this mutation were more likely to survive infection; thus its frequency in the population increased.<ref>{{cite episode |title=Mystery of the Black Death |url=https://www.pbs.org/wnet/secrets/mystery-black-death-background/1488/ |access-date=10 October 2015 |series=[[Secrets of the Dead]] |network=[[PBS]] |date=30 October 2002 |season=3 |number=2 |url-status=live |archive-url=https://web.archive.org/web/20151012175528/http://www.pbs.org/wnet/secrets/mystery-black-death-background/1488/ |archive-date=12 October 2015}} Episode background.</ref> This theory could explain why this mutation is not found in [[Southern Africa]], which remained untouched by bubonic plague. A newer theory suggests that the [[Evolutionary pressure|selective pressure]] on the CCR5 Delta 32 mutation was caused by [[smallpox]] instead of the bubonic plague.<ref>{{cite journal | vauthors = Galvani AP, Slatkin M | title = Evaluating plague and smallpox as historical selective pressures for the CCR5-Delta 32 HIV-resistance allele | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 100 | issue = 25 | pages = 15276–9 | date = December 2003 | pmid = 14645720 | pmc = 299980 | doi = 10.1073/pnas.2435085100 | bibcode = 2003PNAS..10015276G | author-link2 = Montgomery Slatkin | doi-access = free }}</ref>

'''Malaria resistance''': An example of a harmful mutation is [[sickle-cell disease]], a blood disorder in which the body produces an abnormal type of the oxygen-carrying substance [[haemoglobin]] in the [[red blood cell]]s. One-third of all [[Indigenous peoples|indigenous]] inhabitants of [[Sub-Saharan Africa]] carry the allele, because, in areas where [[malaria]] is common, there is a [[Evolution|survival value]] in carrying only a single sickle-cell allele ([[sickle cell trait]]).<ref>{{cite web |url=http://sicklecell.md/faq.asp |title=Frequently Asked Questions [FAQ's] | vauthors = Konotey-Ahulu F |website=sicklecell.md |url-status=dead |archive-url=https://web.archive.org/web/20110430031852/http://sicklecell.md/faq.asp |archive-date=30 April 2011 |access-date=16 April 2010 }}</ref> Those with only one of the two alleles of the sickle-cell disease are more resistant to malaria, since the infestation of the malaria ''[[Plasmodium]]'' is halted by the sickling of the cells that it infests.

'''Antibiotic resistance''': Practically all bacteria develop antibiotic resistance when exposed to antibiotics. In fact, bacterial populations already have such mutations that get selected under antibiotic selection.<ref>{{cite journal | vauthors = Hughes D, Andersson DI | title = Evolutionary Trajectories to Antibiotic Resistance | journal = Annual Review of Microbiology | volume = 71 | pages = 579–596 | date = September 2017 | pmid = 28697667 | doi = 10.1146/annurev-micro-090816-093813 | doi-access = free }}</ref> Obviously, such mutations are only beneficial for the bacteria but not for those infected.

'''[[Lactase persistence]]'''. A mutation allowed humans to express the enzyme [[lactase]] after they are naturally weaned from breast milk, allowing adults to digest [[lactose]], which is likely one of the most beneficial mutations in recent [[human evolution]].<ref>{{cite journal | vauthors = Ségurel L, Bon C | title = On the Evolution of Lactase Persistence in Humans | journal = Annual Review of Genomics and Human Genetics | volume = 18 | pages = 297–319 | date = August 2017 | pmid = 28426286 | doi = 10.1146/annurev-genom-091416-035340 }}</ref>