A review on molecular markers of Plasmodium falciparum.

Abstract

Malaria is an infectious disease caused by parasitic protozoans of the genus Plasmodium. Malaria control efforts on a global scale are in danger due to the emergence and spread of drug-resistant malaria. Despite stakeholders' dedication to the prevention and treatment of malaria, the current state of global health does not offer an effective answer to the issue of drug resistance. Furthermore, there is an information gap about the molecular mechanisms of Plasmodium falciparum's drug resistance, which makes it difficult to develop monitoring systems. Most countries lack adequate and comprehensive information on antimalarial drug efficacy. Plasmodium falciparum has developed resistance to almost all anti-malarial drugs, which poses a significant danger to malaria control worldwide. The fundamental mechanism of artemisinin resistance is due to point mutations in the beta-propeller domain of the gene encoding Kelch protein 13. Atovaquone resistance can be caused by a variety of mutations in the cytochrome b gene, with the majority of mutations affecting the protein's ubiquinol binding site. Similarly, mutations in the Plasmodium falciparum chloroquine resistance transporter, Plasmodium falciparum multi-drug resistance 1, and an increase in Plasmodium falciparum Plasmepsin II and III copy numbers all lead to 4-aminoquinoline drug resistance. Also, the number of amino acid substitutions in dihydrofolate reductase and dihydropteroate synthase is correlated with the degree of antifolate drug resistance. Moreover, amino alcohol drug resistance is caused by Plasmodium falciparum multidrug resistance protein 1 and Plasmodium falciparum Na+/H + exchanger 1 mutations. In general, Plasmodium falciparum chloroquine resistance transporter, Plasmodium falciparum multidrug resistance protein 1, Plasmodium falciparum Na+/H + exchanger 1, plasmepsin II & III, cytochrome b gene, dihydrofolate reductase, Plasmodium falciparum ATPases 6, Plasmodium falciparum Kelch protein 13, and dihydropteroate synthase were just the molecular markers of drug resistance of Plasmodium falciparum. Future research on the molecular mechanisms of drug resistance in P. falciparum should focus on significant area including using transcriptomic and genomic technologies to identify genetic variations associated with resistance. Finding the protein interactions that underlie these resistance mechanisms requires proteomic research. Additionally, the possibility of resistance development may be decreased by investigating combination therapies that target several phases of the P. falciparum lifecycle. In order to successfully address drug resistance in malaria, it will be essential to strengthen worldwide monitoring systems and promote interdisciplinary collaboration among researchers and healthcare professionals. Furthermore, regular monitoring, identification, and limiting of drug-resistant P. falciparum strains through in vivo efficacy tests, in vitro tests, combination therapy, molecular techniques, and appropriate policies must continue to ensure the effectiveness of malaria treatment.