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Inactivation of the miltefosine transporter, LdMT, causes miltefosine resistance that is conferred to the amastigote stage of Leishmania donovani and persists in vivo

AuthorsSeifert, K.; Pérez-Victoria, F. J.; Stettler, M.; Sánchez-Cañete, María P.; Castanys, Santiago; Gamarro, Francisco; Croft, S. L.
Issue Date2007
CitationInternational Journal of Antimicrobial Agents 30: 229- 235 (2007)
AbstractMiltefosine (hexadecylphosphocholine) is the first oral antileishmanial drug. In this study, we addressed the question whether miltefosine-resistant Leishmania donovani promastigotes transform to miltefosine-resistant amastigotes. A promastigote line, M-mutR, showed defective internalisation of miltefosine owing to mutations in LdMT, similar to previously described resistant lines. M-mutR parasites were infective to macrophages in vitro as well as in BALB/c mice in vivo. There was good correlation of in vitro resistance indices between promastigotes and intracellular amastigotes. Most importantly, M-mutR parasites retained the resistant phenotype in vivo, with no decrease of hepatic burden in BALB/c mice following miltefosine treatment up to 30 mg/kg (ca. 90% inhibition in wild-type infections). No cross-resistance to other antileishmanial drugs was observed in M-mutR amastigotes. © 2007 Elsevier B.V. and the International Society of Chemotherapy.
Identifiersdoi: 10.1016/j.ijantimicag.2007.05.007
issn: 0924-8579
Appears in Collections:(IPBLN) Artículos
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