Spread and evolution of Plasmodium falciparum drug resistance

Mita, Toshihiro; Tanabe, Kazuyuki; Kita, Kiyoshi

doi:10.1016/j.parint.2009.04.004

Cited by 223 publications

(214 citation statements)

References 115 publications

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“…Verified cases of positive Darwinian selection in response to human-induced environmental changes have been relatively few, mostly involving drugs, pesticides and other toxins (Mita et al, 2009;Rivero et al, 2010). Rather, the main biotic result of human-induced environmental alteration has been 'a few winners replacing many losers,' in the memorable phrase of McKinney and Lockwood, 1999.…”

Section: Predictionsmentioning

confidence: 99%

Evolution of adaptive phenotypic traits without positive Darwinian selection

Hughes

2011

Heredity

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Recent evidence suggests the frequent occurrence of a simple non-Darwinian (but non-Lamarckian) model for the evolution of adaptive phenotypic traits, here entitled the plasticity-relaxation-mutation (PRM) mechanism. This mechanism involves ancestral phenotypic plasticity followed by specialization in one alternative environment and thus the permanent expression of one alternative phenotype. Once this specialization occurs, purifying selection on the molecular basis of other phenotypes is relaxed. Finally, mutations that permanently eliminate the pathways leading to alternative phenotypes can be fixed by genetic drift. Although the generality of the PRM mechanism is at present unknown, I discuss evidence for its widespread occurrence, including the prevalence of exaptations in evolution, evidence that phenotypic plasticity has preceded adaptation in a number of taxa and evidence that adaptive traits have resulted from loss of alternative developmental pathways. The PRM mechanism can easily explain cases of explosive adaptive radiation, as well as recently reported cases of apparent adaptive evolution over ecological time.

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Section: Predictionsmentioning

confidence: 99%

Evolution of adaptive phenotypic traits without positive Darwinian selection

Hughes

2011

Heredity

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“…Resistance then spread to other SE Asian countries in the following decade [12]. Resistance to chloroquine was later reported in Kenya in 1978 [13] and spread rapidly over Africa, and was firmly established all over the continent south of the Sahara by 1990 [14]. The initial chloroquine-resistant lineage in Africa was CVIET, underlining that the lineage was probably introduced to Africa from SE Asia [14].…”

Section: Monotherapiesmentioning

confidence: 99%

“…Resistance to chloroquine was later reported in Kenya in 1978 [13] and spread rapidly over Africa, and was firmly established all over the continent south of the Sahara by 1990 [14]. The initial chloroquine-resistant lineage in Africa was CVIET, underlining that the lineage was probably introduced to Africa from SE Asia [14]. It has been an open question for decades as to whether chloroquine resistance would revert once chloroquine was abandoned and the drug pressure on the parasite population was thus lifted.…”

Section: Monotherapiesmentioning

confidence: 99%

“…Resistance to SP was first reported from the ThailandCambodian border in the 1960s and spread in the following years to other countries in SE Asia [14,17]. Molecular data suggest that SP resistance in Africa has developed independently of the SE Asian focus in several locations [14].…”

Section: Sulfadoxine/pyrimethaminementioning

confidence: 99%

“…Molecular data suggest that SP resistance in Africa has developed independently of the SE Asian focus in several locations [14]. Resistance to SP caused by mutations in the dihydrofolate reductase and dihydropteroate genes has spread rapidly in all parts of the world, except the Middle East and Central America [18].…”

Section: Sulfadoxine/pyrimethaminementioning

confidence: 99%

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