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Abstract
Leishmaniasis is a protozoan parasitic disease endemic to the tropical and subtropical regions of the world, with three major clinical forms, self-healing cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis (MCL), and visceral leishmaniasis (VL). Drug treatments are expensive and often result in the development of drug resistance. No vaccine is available against leishmaniasis. Subunit Leishmania vaccine immunization in animal models has shown some efficacy but little or none in humans. However, individuals who recover from natural infection are protected from reinfection and develop life-long protection, suggesting that infection may be a prerequisite for immunological memory. Thus, genetically altered live-attenuated parasites with controlled infectivity could achieve such memory. In this paper, we discuss development and characteristics of genetically altered, live-attenuated Leishmania donovani parasites and their possible use as vaccine candidates against VL. In addition, we discuss the challenges and other considerations in the use of live-attenuated parasites.
Highlights
Leishmaniasis is caused by protozoan parasites of the genus Leishmania of the family Trypanosomatidae and is transmitted by the sand fly vector
It infects about 12 million individuals globally in tropical and subtropical regions, with ∼2 million new clinical cases (0.5 million visceral leishmaniasis (VL) and 1.5 million cutaneous leishmaniasis (CL)) reported annually with an estimated death toll of ∼50,000 persons/year [1]
The three major clinical forms of leishmaniasis, VL, CL, and mucocutaneous leishmaniasis (MCL) are the result of infection by different species of the parasite and the immune response of the host
Summary
Leishmaniasis is caused by protozoan parasites of the genus Leishmania of the family Trypanosomatidae and is transmitted by the sand fly vector It infects about 12 million individuals globally in tropical and subtropical regions, with ∼2 million new clinical cases (0.5 million visceral leishmaniasis (VL) and 1.5 million cutaneous leishmaniasis (CL)) reported annually with an estimated death toll of ∼50,000 persons/year [1]. Parasites are taken up by the neutrophils that are ingested by the host macrophages, differentiate into the nonmotile amastigote form, and reside and multiply in the phagolysosome compartment of the macrophages These two major life stages have been adapted to in vitro culture for most Leishmania species allowing manipulation of the genome and assessment of the altered phenotypes in vitro and in vivo. In this paper we have limited our scope to genetically altered L. donovani parasites and their use as vaccine candidates
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