Why has the dihydrofolate reductase 164 mutation not consistently been found in Africa yet?
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Date
2005Author
Marsh, Kevin
Ward, Steve
Winstanley, Peter
Gilbert, Kokwaro
Nduati, Eunice
Ochong, Edwin
Nzila, Alexis
Type
ArticleLanguage
enMetadata
Show full item recordAbstract
Resistance to the antifolate sulfadoxine–pyrimethamine (SP), the current mass-treatment antimalarial drug, is associated with selection of point mutations in dihydrofolate reductase and dihydropteroate synthase. Among these mutations, the leucine 164 dihydrofolate reductase mutation (Leu-164) is associated with higher levels of SP resistance; this mutation is also associated with a decrease in the efficacy of chlorproguanil/dapsone, a newly developed antifolate antimalarial drug. Leu-164 has been detected in Southeast Asia and South America, regions where SP is no longer effective. Surprisingly, this mutation has not yet been detected in Africa, using the standard protocol based on PCR–RFLP, despite high SP resistance. In this paper, we discuss briefly the reasons why Leu-164 has not yet been selected in Africa and we propose a means that may slow down the selection of this mutation.
URI
http://trstmh.oxfordjournals.org/content/99/5/341.shorthttp://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/47334
Citation
Trans R Soc Trop Med Hyg (2005) 99 (5): 341-346Publisher
Department of Pharmaceutics and Pharmacy Practice
Collections
- Faculty of Health Sciences (FHS) [10378]