Editing Plasmodium falciparum (section)

== Influence on the human genome ==
{{Further|Genetic resistance to malaria}}
The high [[death|mortality]] and [[morbidity]] caused by ''P.&nbsp;falciparum'' has placed great [[Selection (biology)|selective pressure]] on the [[human genome]]. Several genetic factors provide [[genetic resistance to malaria|some resistance to ''Plasmodium'' infection]], including [[sickle cell trait]], [[thalassaemia]] traits, [[glucose-6-phosphate dehydrogenase deficiency]], and the absence of [[Duffy antigen]]s on red blood cells.<ref name="Kwiatkowski 2005">{{Cite journal |author=Kwiatkowski DP |title=How malaria has affected the human genome and what human genetics can teach us about malaria |journal=American Journal of Human Genetics |volume=77 |issue=2 |pages=171–92 |year=2005 |pmid=16001361 |pmc=1224522 |doi=10.1086/432519}} {{open access}}</ref><ref name="Hedrick 2011">{{Cite journal |author=Hedrick PW |title=Population genetics of malaria resistance in humans |journal=Heredity |year=2011 |volume=107 |issue=4 |pages=283–304 |pmid=21427751 |doi=10.1038/hdy.2011.16 |pmc=3182497}} {{open access}}</ref> E. A. Beet, a doctor working in [[Southern Rhodesia]] (now [[Zimbabwe]]) had observed in 1948 that [[sickle-cell disease]] was related to a lower rate of malaria infections.<ref>{{cite journal|last1=Beet|first1=EA|title=Sickle cell disease in the Balovale District of Northern Rhodesia|journal=East African Medical Journal|date=1946|volume=23|pages=75–86|pmid=21027890}}</ref> This suggestion was reiterated by [[J. B. S. Haldane]] in 1948, who suggested that [[thalassaemia]] might provide similar protection.<ref>{{cite journal|last1=Hedrick|first1=P W|title=Population genetics of malaria resistance in humans|journal=Heredity|date=2011|volume=107|issue=4|pages=283–304|doi=10.1038/hdy.2011.16|pmid=21427751|pmc=3182497}}</ref> This hypothesis has since been confirmed and extended to [[hemoglobin E]]<ref>{{cite journal|last1=Chotivanich|first1=K|last2=Udomsangpetch|first2=R|last3=Pattanapanyasat|first3=K|last4=Chierakul|first4=W|last5=Simpson|first5=J|last6=Looareesuwan|first6=S|last7=White|first7=N|title=Hemoglobin E: a balanced polymorphism protective against high parasitemias and thus severe P falciparum malaria.|journal=Blood|date=2002|volume=100|issue=4|pages=1172–6|pmid=12149194|doi=10.1182/blood.V100.4.1172.h81602001172_1172_1176|doi-access=free}}</ref> and [[hemoglobin C]].<ref>{{cite journal|last1=Verra|first1=Federica|last2=Simpore|first2=Jacques|last3=Warimwe|first3=George M.|last4=Tetteh|first4=Kevin K.|last5=Howard|first5=Tevis|last6=Osier|first6=Faith H. A.|last7=Bancone|first7=Germana|last8=Avellino|first8=Pamela|last9=Blot|first9=Isa|last10=Fegan|first10=Greg|last11=Bull|first11=Peter C.|last12=Williams|first12=Thomas N.|last13=Conway|first13=David J.|last14=Marsh|first14=Kevin|last15=Modiano|first15=David|last16=Hall|first16=Neil|title=Haemoglobin C and S Role in Acquired Immunity against ''Plasmodium falciparum'' Malaria|journal=PLOS ONE|date=3 October 2007|volume=2|issue=10|pages=e978|doi=10.1371/journal.pone.0000978|pmid=17912355|pmc=1991593|display-authors=8|bibcode=2007PLoSO...2..978V|doi-access=free}}</ref>