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Overexpression of a single Leishmania major gene enhances parasite infectivity in vivo and in vitro.

Reiling L, Chrobak M, Schmetz C, Clos J

  • Journal Molecular microbiology

  • Published 25 Mar 2010

  • Volume 76

  • ISSUE 5

  • Pagination 1175-90

  • DOI 10.1111/j.1365-2958.2010.07130.x


We identified a Leishmania major-specific gene that can partly compensate for the loss of virulence observed for L. major HSP100 null mutants. The gene, encoding a 46 kD protein of unknown function and lineage, also enhances the virulence of wild type L. major upon overexpression. Surprisingly, the approximately sixfold overexpression of this protein also extends the host range of L. major to normally resistant C57BL/6 mice, causing persisting lesions in this strain, even while eliciting a strong cellular immune response. This enhanced virulence in vivo is mirrored in vitro by increased parasite burden inside bone marrow-derived macrophages. The localization of the protein in the macrophage cytoplasm suggests that it may modulate the macrophage effector mechanisms. In summary, our data show that even minor changes of gene expression in L. major may alter the outcome of an infection, regardless of the host's genetic predisposition.