@article{fdi:010055942,
  title = {{M}olecular monitoring of {P}lasmodium falciparum drug susceptibility at the time of the introduction of artemisinin-based combination therapy in {Y}aounde, {C}ameroon : implications for the future},
  author = {{M}{\'e}nard, {S}. and {M}orlais, {I}sabelle and {T}ahar, {R}achida and {S}ayang, {C}. and {M}ayengue, {P}. {I}. and {I}riart, {X}. and {B}enoit-{V}ical, {F}. and {L}emen, {B}. and {M}agnaval, {J}. {F}. and {A}wono-{A}mbene, {P}. and {B}asco, {L}eonardo and {B}erry, {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{B}ackground: {R}egular monitoring of the levels of anti-malarial resistance of {P}lasmodium falciparum is an essential policy to adapt therapy and improve malaria control. {T}his monitoring can be facilitated by using molecular tools, which are easier to implement than the classical determination of the resistance phenotype. {I}n {C}ameroon, chloroquine ({CQ}), previously the first-line therapy for uncomplicated malaria was officially withdrawn in 2002 and replaced initially by amodiaquine ({AQ}) monotherapy. {T}hen, artemisinin-based combination therapy ({ACT}), notably artesunate-amodiaquine ({AS}-{AQ}) or artemether-lumefantrine ({AL}), was gradually introduced in 2004. {T}his situation raised the question of the evolution of {P}. falciparum resistance molecular markers in {Y}aounde, a highly urbanized {C}ameroonian city. {M}ethods: {T}he genotype of pfcrt 72 and 76 and pfmdr1 86 alleles and pfmdr1 copy number were determined using real-time {PCR} in 447 {P}. falciparum samples collected between 2005 and 2009. {R}esults: {T}his study showed a high prevalence of parasites with mutant pfcrt 76 (83%) and pfmdr1 86 (93%) codons. {O}n the contrary, no mutations in the pfcrt 72 codon and no samples with duplication of the pfmdr1 gene were observed. {C}onclusion: {T}he high prevalence of mutant pfcrt 76{T} and pfmdr1 86{Y} alleles might be due to the choice of alternative drugs ({AQ} and {AS}-{AQ}) known to select such genotypes. {M}utant pfcrt 72 codon was not detected despite the prolonged use of {AQ} either as monotherapy or combined with artesunate. {T}he absence of pfmdr1 multicopies suggests that {AL} would still remain efficient. {T}he limited use of mefloquine or the predominance of mutant pfmdr1 86{Y} codon could explain the lack of pfmdr1 amplification. {I}ndeed, this mutant codon is rarely associated with duplication of pfmdr1 gene. {I}n {C}ameroon, the changes of therapeutic strategies and the simultaneous use of several formulations of {ACT} or other anti-malarials that are not officially recommended result in a complex selective pressure, rendering the prediction of the evolution of {P}. falciparum resistance difficult. {T}his public health problem should lead to increased vigilance and regular monitoring.},
  keywords = {{M}alaria ; {C}ameroon ; pfcrt ; pfmdr1 ; pfmdr1 copy number ; {R}esistance ; {LNA} ; probes},
  booktitle = {},
  journal = {{M}alaria {J}ournal},
  volume = {11},
  numero = {1},
  pages = {113},
  ISSN = {1475-2875},
  year = {2012},
  DOI = {10.1186/1475-2875-11-113},
  URL = {https://www.documentation.ird.fr/hor/fdi:010055942},
}