Polimorfizmi crvenih krvnih stanica i adaptacija na malariju

undergraduate thesis

• Title (english): Red blood cell polymorphisms and adaptation to malaria
• Author: Jasmina Puhović
• Mentor: Mirjana Pavlica (mentor)
• Granter: University of Zagreb; Faculty of Science; (Department of Biology); Zagreb
• Defense date and country: 2009, Croatia
• Scientific / art field, discipline and subdiscipline: NATURAL SCIENCES; Biology

Abstract

Malarija je zarazna bolest koju uzrokuju paraziti iz roda Plasmodium, a prenose je komarci iz roda Anopheles. Mortalitet je dosta visok unatoč postojanju lijekova protiv malarije jer si ljudi koji žive u područjima s endemičnom malarijom često ne mogu priuštiti liječenje. Smatra se da je malarija najjača sila prirodne selekcije poznata u novijoj povijesti ljudskog genoma. Pod selekcijskim pritiskom, u različitim populacijama endemičnih područja nastale su brojne genske promjene koje pružaju neku vrstu zaštite od malarije, a najčešće sprječavaju razvoj teškog oblika bolesti. Najpoznatiji primjer je srpasta anemija, nasljedna bolest koja je raširena u područjima s endemičnom malarijom, a heterozigoti nemaju simptome bolesti niti malarije. Crvene krvne stanice, eritrociti, sudjeluju u najvažnijem dijelu životnog ciklusa plazmodija, jer opskrbljuju parazita hranom i kisikom i pružaju mu zaštitu. Zaštitni polimorfizmi najčešće se odnose na gene koji utječu na strukturu ili funkciju eritrocita. To su npr. strukturne varijante hemoglobina: HbS, HbC, HbE; talasemija, ovalocitoza, promjene enzima crvenih krvnih stanica, npr. nedostatak G6PD, i antigeni na površini eritrocita kao što su Duffy-antigen, glikoproteini, receptori za komplemente i PfEMP1. Proučavanje tih genskih varijabilnosti važno je za otkrivanje interakcija između parazita i ljudskih stanica, što bi se u budućnosti moglo iskoristiti za stvaranje učinkovitih i dostupnih cjepiva ili lijekova protiv malarije.

Abstract (english)

Malaria is an infectious disease caused by protozoan parasites of the genus Plasmodium and it is transmitted by musquitoes of the genus Anopheles. Although there are antimalarial drugs, mortality levels are very high because drug treatments are often too expensive for people living in malaria endemic areas. Malaria is probably the greatest selective pressure on the human genome in recent history. This pressure has resulted in number of genetic variants that confer some kind of protection against the malaria, they are mostly protective against severe form of the disease. The most-studied condition is the sickle-cell disease, a hereditary blood disease present in malaria-endemic regions. Heterozygotes have no symptoms of the disease nor severe malaria. Red blood cells are involved in the most important part of plasmodium life cycle because they provide the parasite with food, oxygen and shelter. Malaria resistance genes are mostly those that determine the red blood cell structure or function. Red blood cell polymorphisms associated with some protection are the structural haemoglobin variants like sickle cell trait or disease, HbC and HbE; thalassemia, ovalocytosis, changes in red blood cell enzymes like G6PD deficiency and red blood cell surface antigens like Duffy antigens, glycoproteins, complement receptors and PfEMP1. Studying those genetic variants is important because it can teach us about protective relationship between human cells and malaria. In the future, that knowledge might be used for the development of effective and affordable vaccines or anti-malarial drugs.

• Keywords: malarija; crvene krvne stanice; eritrociti
• Keywords (english): malaria; red blood cells; erythrocytes
• Language: croatian
• URN:NBN: urn:nbn:hr:217:752133
• Study programme: Title: Ecology; Study programme type: university; Study level: undergraduate; Academic / professional title: sveučilišni/a prvostupnik/prvostupnica (baccalaureus/baccalaurea) biologije (sveučilišni/a prvostupnik/prvostupnica (baccalaureus/baccalaurea) biologije)
• Type of resource: Text
• File origin: Born digital
• Access conditions: Open access
• Created on: 2018-03-15 11:03:57