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THE OMPA-LIKE PROTEIN LOA22 IS ESSENTIAL FOR LEPTOSPIRAL VIRULENCE
Author
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Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France / Universidade Federal do Rio de Janeiro. Instituto de Microbiologia Professor Paulo de Goes. Rio de Janeiro, RJ, Brasil
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Institut Pasteur. Unité de Recherche et d’Expertise Histotechnologie et Pathologie. Paris, France
Institut Pasteur. Unité de Recherche et d’Expertise Histotechnologie et Pathologie. Paris, France
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Weill Medical College of Cornell University. Division of International Medicine and Infectious Disease. New York, New York, USA
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Institut Pasteur. Unité de Recherche et d’Expertise Histotechnologie et Pathologie. Paris, France
Institut Pasteur. Unité de Recherche et d’Expertise Histotechnologie et Pathologie. Paris, France
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / Weill Medical College of Cornell University. Division of International Medicine and Infectious Disease. New York, New York, USA
Institut Pasteur. Unité de Biologie des Spirochètes. Paris, France
Abstract
Pathogenic mechanisms of Leptospira interrogans, the causal agent of leptospirosis, remain largely unknown. This is
mainly due to the lack of tools for genetic manipulations of pathogenic species. In this study, we characterized a
mutant obtained by insertion of the transposon Himar1 into a gene encoding a putative lipoprotein, Loa22, which has
a predicted OmpA domain based on sequence identity. The resulting mutant did not express Loa22 and was
attenuated in virulence in the guinea pig and hamster models of leptospirosis, whereas the genetically complemented
strain was restored in Loa22 expression and virulence. Our results show that Loa22 was expressed during host
infection and exposed on the cell surface. Loa22 is therefore necessary for virulence of L. interrogans in the animal
model and represents, to our knowledge, the first genetically defined virulence factor in Leptospira species
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