Abstract
1Laboratory for Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium, 2Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium,3Operational Research Unit, Medical Department, Me´decins Sans Frontie`res – Operational Centre Brussels, Brussels, Belgium, 4Department of Pharmaceutical andPharmacological Sciences, Katholieke Universiteit Leuven, Leuven, Belgium, 5Faculty of Medicine, Addis Ababa University, Addis Ababa, Ethiopia, 6Department of ClinicalSciences, Institute of Tropical Medicine, Antwerp, Belgium
Highlights
Visceral leishmaniasis (VL) is a disseminated protozoan infection caused by the Leishmania donovani spp. complex and is transmitted by phlebotomine sand flies
While human immunodeficiency virus (HIV)-VL coinfection is associated with accelerated HIV and VL progression and a poor prognosis, it appears to be governed by a number of unique and poorly explained features
The observed therapeutic failure contrasts sharply with, e.g., the immune reconstitution inflammatory syndrome (IRIS) events observed in other coinfections, which—while detrimental—are indicative of a partial and possibly even over-exuberant restoration of pathogenspecific immune responses [2]
Summary
Visceral leishmaniasis (VL) is a disseminated protozoan infection caused by the Leishmania donovani spp. complex and is transmitted by phlebotomine sand flies. One of these unique features is that even after virological suppression under antiretroviral therapy (ART), patients often remain clinically and immunologically in a state of immunodeficiency and anergy, with diffuse organ spread of parasites [1,3].
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