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. 2010 Sep;2(3):248-57.
doi: 10.4103/0974-777X.68528.

Human immunodeficiency virus and leishmaniasis

Navid Ezra  1 , Maria Teresa Ochoa, Noah Craft
Affiliations

Human immunodeficiency virus and leishmaniasis

Navid Ezra et al. J Glob Infect Dis. 2010 Sep.

Abstract

The Leishmaniases are a group of diseases transmitted to humans by the bite of a sandfly, caused by protozoan parasites of the genus Leishmania. Various Leishmania species infect humans, producing a spectrum of clinical manifestations. It is estimated that 350 million people are at risk, with a global yearly incidence of 1-1.5 million for cutaneous and 500,000 for visceral Leishmaniasis (VL). VL is a major cause of morbidity and mortality in East Africa, Brazil and the Indian subcontinent. Co-infection with human immunodeficiency virus (HIV) alters the immune response to the disease. Here we review the immune response to Leishmania in the setting of HIV co-infection. Improved understanding of the immunology involved in co-infections may help in designing prophylactic and therapeutic strategies against Leishmaniasis.

Keywords: AIDS; Co-infection; HIV; Immunology; Leishmaniasis.

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Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
The immunology of resolving infection and disease progression to Leishmania For both T helper 1 (TH1)- and TH2-cell differentiations, antigens are presented to naive CD4+ T cells by dendritic cells (DCs). The interaction of co-stimulatory molecules with their respective ligands, together with the local cytokine environment, promotes the differentiation of naive T cells into interferon- γ (IFN-γ)-secreting TH1 cells or interleukin-4 (IL-4)-secreting TH2 cells. In TH1-cell development, certain pathogens or pathogen-associated molecular patterns (PAMPs) trigger antigen-presenting cells, through toll-like receptors (TLRs), to secrete IL-12, which promotes the differentiation of naive T cells into IFN-γ-secreting TH1 cells. In TH2-cell development, the inability of antigen to activate DCs to produce IL-12 results in a default pathway of naive T-cell differentiation into IL-4-secreting TH2 cells
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