Leishmania, RNA virus, virulence, innate immunity
I am full professor at the Faculty of Biology and Medicine at the University of Lausanne. After studying biology at the University of Fribourg (Switzerland) and obtaining a doctoral degree at the Swiss Institute for Experimental Cancer Research working on mouse mammary tumor virus, I took up a post-doctoral position at the University of California Los Angeles working on immunoglobulin gene regulation. On my return to Switzerland, I studied post-translational modifications of cell surface antigens. As an independant researcher of the Dr. Max Cloëtta Research Foundation, I had the opportunity to establish my own group investigating the molecular and cellular biology of protozoan parasites. My more recent research focuses on the host-pathogen interaction and the impact of co-infections. From 2003 to 2016, I directed the Department of Biochemistry of the Faculty and since August 2015 I have been the Vice-Dean for Research and Innovation of the Faculty of Biology and Medicine.
My research interests include Leishmania. As veterans of infection, Leishmania guyanensis parasites have been plaguing humankind for centuries, provoking a deleterious hyper-inflammatory immune response, destroying host tissue and forming the ulcerating lesions, which typify most forms of the disease. About 15% of patients develop secondary lesions in the mouth and nose, where parasites metastasise to mucocutaneous tissues creating debilitating and exceptionally disfiguring inflammation.
Our lab has recently shown that a virus within metastatic Leishmania parasites (Leishmania RNA virus: LRV) can act as an independently immunogenic entity, where its RNA-based nucleic acid acted as a potent innate immunogen, triggering a destructive hyper-inflammatory cascade through Toll-Like-Receptor 3 recognition and inducing metastasis of the infection. We dub this process “hyperpathogenism” and have exposed its importance as a major clinical consideration in metastatic leishmaniasis. Based on these results, we further demonstrated that concomitant, or subsequent infection by other viruses, can similarly exacerbate Leishmania pathogenicity and lead to relapse of infection.
By appreciating the microbial-virus as a backseat driver of human disease, we may be able to better formulate appropriate clinical interventions or even exploit its presence for clinical benefit. Further, viral presence or co-infections could act as biomarkers, guiding diagnostics, treatment and phylogenetics, and have potential as novel molecular targets for therapeutic and prophylactic interventions to prevent hyperpathogenicity.
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