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Searching for virulence factors in the non-pathogenic parasite to humans Leishmania tarentolae

Published online by Cambridge University Press:  06 May 2009

H. AZIZI
Affiliation:
Molecular Immunology and Vaccine Research Laboratory, Pasteur Institute of Iran, Tehran, Iran
K. HASSANI
Affiliation:
Molecular Immunology and Vaccine Research Laboratory, Pasteur Institute of Iran, Tehran, Iran Department of Biotechnology, University College of Science, University of Tehran, Tehran, Iran
Y. TASLIMI
Affiliation:
Molecular Immunology and Vaccine Research Laboratory, Pasteur Institute of Iran, Tehran, Iran
H. SHATERI NAJAFABADI
Affiliation:
Institute of Parasitology, McGill University, Montreal, Canada
B. PAPADOPOULOU
Affiliation:
Research Centre in Infectious Diseases, CHUL Research Centre and Department of Medical Biology, Faculty of Medicine, Laval University, 2705 Laurier Blvd., Quebec (QC), CanadaG1V 4G2
S. RAFATI*
Affiliation:
Molecular Immunology and Vaccine Research Laboratory, Pasteur Institute of Iran, Tehran, Iran
*
*Corresponding author: Molecular Immunology and Vaccine Research Laboratory, Pasteur Institute of Iran, Tehran, Iran. Tel: +98 21 66953311. Fax: +98 21 66465132. E-mail: [email protected] or [email protected]

Summary

Leishmania protozoa are obligate intracellular parasites that reside in the phagolysosome of host macrophages and cause a large spectrum of pathologies to humans known as leishmaniases. The outcome of the disease is highly dependent on the parasite species and on its ascribed virulence factors and the immune status of the host. Characterization of the genome composition of non-pathogenic species could ultimately open new horizons in Leishmania developmental biology and also the disease monitoring. Here, we provide evidence that the lizard non-pathogenic to humans Leishmania tarentolae species expresses an Amastin-like gene, cysteine protease B (CPB), lipophosphoglycan LPG3 and the leishmanolysin GP63, genes well-known for their potential role in the parasite virulence. These genes were expressed at levels comparable to those in L. major and L. infantum both at the level of mRNA and protein. Alignment of the L. tarentolae proteins with their counterparts in the pathogenic species demonstrated that the degree of similarity varied from 59% and 60% for Amastin, 89% for LPG3 and 71% and 68% for CPB, in L. major and L. infantum, respectively. Interestingly, the A2 gene, expressed specifically by the L. donovani complex which promotes visceralization, was absent in L. tarentolae. These findings suggest that the lack of pathogenicity in L. tarentolae is not associated with known virulence genes such as LPG3, CPB, GP63 and Amastin, and that other factors either unique to L. tarentolae or missing from this species may be responsible for the non-pathogenic potential of this lizard parasite.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2009

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