The immunology of Leishmania/HIV co-infection

Ifeoma Okwor, Jude Eze Uzonna

Leishmaniases are emerging as an important disease in human immunodeficiency virus (HIV)-infected persons living in several sub-tropical and tropical regions around the world, including the Mediterranean. The HIV/AIDS pandemic is spreading at an alarming rate in Africa and the Indian subcontinent, areas with very high prevalence of leishmaniases. The spread of HIV into rural areas and the concomitant spread of leishmaniases to suburban/urban areas have helped maintain the occurrence of Leishmania/HIV co-infection in many parts of the world. The number of cases of Leishmania/HIV co-infection is expected to rise owing to the overlapping geographical distribution of the two infections. In Southwestern Europe, there is also an increasing incidence of Leishmania/HIV co-infection (particularly visceral leishmaniasis) in such countries as France, Italy, Spain and Portugal. Studies suggest that in humans, very complex mechanisms involving dysregulation of host immune responses contribute to Leishmania-mediated immune activation and pathogenesis of HIV. In addition, both HIV-1 and Leishmania infect and multiply within cells of myeloid or lymphoid origin, thereby presenting a perfect recipe for reciprocal modulation of Leishmania and HIV-1-related disease pathogenesis. Importantly, because recovery from leishmaniases is associated with long-term persistence of parasites at the primary infection sites and their draining lymph nodes, there is very real possibility that HIV-mediated immunosuppression (due to CD4(+) T cell depletion) could lead to reactivation of latent infections (reactivation leishmaniasis) in immunocompromised patients. Here, we present an overview of the immunopathogenesis of Leishmania/HIV co-infection and the implications of this interaction on Leishmania and HIV disease outcome.