Georgia
The study of the polymerase theta gene (Pol-Q) and it's impact on how the Plasmodium Falciparum variant of the Malaria Parasite repairs damage to DNA.
The study of the polymerase theta gene (Pol-Q) and it's impact on how the Plasmodium Falciparum variant of the Malaria Parasite repairs damage to DNA.
Malaria consistently infects on average 282 million people yearly, and more than 610,000 cases result in death. This represents a significant increase in fatalities over the last two years after many years of progressive decline. These high infection rates put malaria as one of the most severe public health problems. Out of the five species that infect humans, Plasmodium falciparum is the most deadly and accounts for the majority of the mortality in children under five in sub-Saharan Africa, as it possesses an ability to undergo a clonal antigenic variation, allowing the parasite to evade the immune system. This causes malaria’s high likelihood of repeatedly sickening patients. As our immune system kills off most of the Plasmodium cells, the antigenic switch allows a relatively small number of remaining parasites to cause another spike. The gene investigated in this experiment was the polymerase theta (Pol-Q) gene. CRISPR-Cas9 technology was used to target the Pol-Q. I found that disrupting the gene in the parasite significantly affected its survival. To confirm these results, implying Pol-Q is an essential gene, I used a subtype of this technology, called a regulatable Cas9. Instead of immediately disrupting the gene, a regulatable Cas9 gives scientists the control to determine when the technology will start working, thus controlling when the gene is disrupted. Using a regulatable Cas9, my results showed that the Pol-Q gene is indeed essential in the Plasmodium falciparum malaria parasite. These findings could be used in future malaria treatment to terminate the relapse cycle that keeps many patients infected.
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2nd place Finalist in Microbiology at the Terra STEM NYC Fair 2026