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J Med Microbiol 56 (2007), 143-153; DOI: 10.1099/jmm.0.46841-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Review

Molecular mechanisms of antimony resistance in Leishmania

Ashutosh1, Shyam Sundar2 and Neena Goyal1

1 Division of Biochemistry, Central Drug Research Institute, Lucknow-226001 (UP) India

2 Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

Correspondence
Neena Goyal
neenacdri{at}yahoo.com


Leishmaniasis causes significant morbidity and mortality worldwide. The disease is endemic in developing countries of tropical regions, and in recent years economic globalization and increased travel have extended its reach to people in developed countries. In the absence of effective vaccines and vector-control measures, the main line of defence against the disease is chemotherapy. Organic pentavalent antimonials [Sb(V)] have been the first-line drugs for the treatment of leishmaniasis for the last six decades, and clinical resistance to these drugs has emerged as a primary obstacle to successful treatment and control. A multiplicity of resistance mechanisms have been described in resistant Leishmania mutants developed in vitro by stepwise increases of the concentration of either antimony [Sb(III)] or the related metal arsenic [As(III)], the most prevalent mechanism being upregulated Sb(III) detoxification and sequestration. With the availability of resistant field isolates, it has now become possible to elucidate mechanisms of clinical resistance. The present review describes the mechanisms of antimony resistance in Leishmania and highlights the links between previous hypotheses and current developments in field studies. Unravelling the molecular mechanisms of clinical resistance could allow the prevention and circumvention of resistance, as well as rational drug design for the treatment of drug-resistant Leishmania.






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