@article{fdi:010064060, title = {{M}olecular epidemiology of drug-resistant {P}lasmodium falciparum in {B}enguela province, {A}ngola}, author = {{N}gane, {V}. {F}. and {D}jaman, {J}. {A}. and {C}uleux, {C}. and {P}iette, {N}. and {C}arnevale, {P}ierre and {B}esnard, {P}. and {F}ortes, {F}. and {B}asco, {L}eonardo and {T}ahar, {R}achida}, editor = {}, language = {{ENG}}, abstract = {{B}ackground: {T}he malaria situation has been worsening in {A}ngola, partly due to armed conflict until the recent past and drug-resistant {P}lasmodium falciparum. {M}alaria transmission is heterogeneous within the country, and data on drug-resistant malaria in different parts of the country are incomplete. {T}he aim of the present study was to evaluate resistance to 4-aminoquinolines and antifolate drugs in {P}. falciparum isolates collected in {B}enguela province, central {A}ngola, using molecular markers. {M}ethods: {F}ingerprick capillary blood was collected from asymptomatic children aged less than 15 years old during a household survey in and around {B}alombo town in 2010-2011. {S}amples were screened for {P}. falciparum by nested {PCR}. {M}olecular markers ({P}. falciparum dihydrofolate reductase [pfdhfr], {P}. falciparum dihydropteroate synthase [pfdhps], {P}. falciparum chloroquine resistance transporter [pfcrt], and {P}. falciparum multidrug-resistance gene 1 [pfmdr1]) were sequenced to determine the key codons associated with drug resistance. {R}esults: {A} total of 60 blood samples were positive for {P}. falciparum. {M}ost isolates with successful {PCR} amplification had mutant pfdhfr alleles, with either double mutant {AICNI} (69%) or triple mutant {AIRNI} (21%) haplotypes. {A}16{V}, {S}108{T}, and {I}164{L} substitutions were not found. {M}any of the isolates were carriers of either {SGKAA} (60%) or {AGKAA} (27%) pfdhps haplotype. {K}540{E} substitution was absent. {T}here were only two pfcrt haplotypes: wild-type {CVMNK} (11%) and mutant {CVIET} (89%). {W}ild-type pfmdr1 {NYSND} haplotype was found in 19% of the isolates, whereas single mutant pfmdr1 {YYSND} and {NFSND} haplotypes occurred in 48% and 11%, respectively. {D}ouble mutant pfmdr1 haplotypes ({YFSND} and {YYSNY}) occurred rarely. {C}onclusions: {T}he results suggest that the high prevalence of mutant pfcrt {CVIET} haplotype is in agreement with low clinical efficacy of chloroquine observed in earlier studies and that the double pfdhfr mutant {AICNI} and single pfdhps mutant {SGKAA} are currently the predominant haplotypes associated with antifolate resistance in {B}enguela province. {T}he hallmark of clinical resistance observed in {E}ast {A}frica, i.e. triple pfdhfr mutant haplotype ({AIRNI}) and double pfdhps mutant haplotype ({SGEAA}), was absent. {T}hese molecular findings need to be further evaluated in parallel with clinical studies, in particular with the efficacy of intermittent preventive treatment using sulphadoxine-pyrimethamine in pregnant women and artesunate-amodiaquine for uncomplicated malaria.}, keywords = {{P}lasmodium falciparum ; {D}rug resistance ; {A}ntifolate drugs ; {C}hloroquine ; {M}olecular markers ; {ANGOLA}}, booktitle = {}, journal = {{M}alaria {J}ournal}, volume = {14}, numero = {}, pages = {art. 113 [6 p.]}, ISSN = {1475-2875}, year = {2015}, DOI = {10.1186/s12936-015-0634-2}, URL = {https://www.documentation.ird.fr/hor/fdi:010064060}, }