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Leishmania and human immunodeficiency virus coinfection: the first 10 years.

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TLDR
Over 850 Leishmania-human immunodeficiency virus (HIV) coinfection cases have been recorded, the majority in Europe, where 7 to 17% of HIV-positive individuals with fever have amastigotes, suggesting that Leishmanniasis-infected individuals without symptoms will express symptoms of leishmaniasis if they become immunosuppressed.
Abstract
Over 850 Leishmania-human immunodeficiency virus (HIV) coinfection cases have been recorded, the majority in Europe, where 7 to 17% of HIV-positive individuals with fever have amastigotes, suggesting that Leishmania-infected individuals without symptoms will express symptoms of leishmaniasis if they become immunosuppressed. However, there are indirect reasons and statistical data demonstrating that intravenous drug addiction plays a specific role in Leishmania infantum transmission: an anthroponotic cycle complementary to the zoonotic one has been suggested. Due to anergy in patients with coinfection, L. infantum dermotropic zymodemes are isolated from patient viscera and a higher L. infantum phenotypic variability is seen. Moreover, insect trypanosomatids that are currently considered nonpathogenic have been isolated from coinfected patients. HIV infection and Leishmania infection each induce important analogous immunological changes whose effects are multiplied if they occur concomitantly, such as a Th1-to-Th2 response switch; however, the consequences of the viral infection predominate. In fact, a large proportion of coinfected patients have no detectable anti-Leishmania antibodies. The microorganisms share target cells, and it has been demonstrated in vitro how L. infantum induces the expression of latent HIV-1. Bone marrow culture is the most useful diagnostic technique, but it is invasive. Blood smears and culture are good alternatives. PCR, xenodiagnosis, and circulating-antigen detection are available only in specialized laboratories. The relationship with low levels of CD4+ cells conditions the clinical presentation and evolution of disease. Most patients have visceral leishmaniasis, but asymptomatic, cutaneous, mucocutaneous, diffuse cutaneous, and post-kala-azar dermal leishmaniasis can be produced by L. infantum. The digestive and respiratory tracts are frequently parasitized. The course of coinfection is marked by a high relapse rate. There is a lack of randomized prospective treatment trials; therefore, coinfected patients are treated by conventional regimens. Prophylactic therapy is suggested to be helpful in preventing relapses.

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Citations
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CD4 + CD25 + regulatory T cells control Leishmania major persistence and immunity

TL;DR: It is shown that the persistence of Leishmania major in the skin after healing in resistant C57BL/6 mice is controlled by an endogenous population of CD4+CD25+ regulatory T cells, indicating that the equilibrium established between effector and regulatory T Cells in sites of chronic infection might reflect both parasite and host survival strategies.
Journal ArticleDOI

Visceral leishmaniasis: what are the needs for diagnosis, treatment and control?

TL;DR: Millefosine, paromomycin and liposomal amphotericin B are gradually replacing pentavalent antimonials and conventional amphoteric in B as the preferred treatments in some regions, but in other areas these drugs are still being evaluated in both mono- and combination therapies.
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Drug Resistance in Leishmaniasis

TL;DR: It is essential that there be a strategy to prevent the emergence of resistance to new drugs; combination therapy, monitoring of therapy, and improved diagnostics could play an essential role in this strategy.
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The increase in risk factors for leishmaniasis worldwide.

TL;DR: Increasing risk factors are making leishmaniasis a growing public health concern for many countries around the world, and some are related to a specific eco-epidemiological entity, others affect all forms of leish maniasis.
References
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Journal ArticleDOI

Abnormalities of B-cell activation and immunoregulation in patients with the acquired immunodeficiency syndrome.

TL;DR: The scope of immune dysfunction in the acquired immunodeficiency syndrome involves B cells as well as T cells, and it is concluded that the manifestations of B-cell hyperreactivity, such as hypergammaglobulinemia, seen in these patients are due to an in vivo polyclonal activation of B cells.
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A TH1→TH2 switch is a critical step in the etiology of HIV infection

TL;DR: This viewpoint proposes that an imbalance in the TH1-type and TH2-type responses contributes to the immune dysregulation associated with HIV infection, and that resistance to HIV infection and/or progression to AIDS is dependent on a TH1-->TH2 dominance.
Journal ArticleDOI

The regulation of immunity to Leishmania major.

TL;DR: Use of the murine L. major model continues to elucidate new methods for vaccine development and suggests a promising system for identification of genes that determine susceptibility to infection.
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Cytokine-induced expression of HIV-1 in a chronically infected promonocyte cell line.

TL;DR: A model system for cytokine-induced up-regulation of human immunodeficiency virus type 1 (HIV-1) expression in chronically infected promonocyte clones was established and can be used to delineate the potential mechanisms whereby HIV-1 infection regulates cellular gene expression.
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Tumor necrosis factor alpha induces expression of human immunodeficiency virus in a chronically infected T-cell clone.

TL;DR: Transient-transfection experiments demonstrated that the inductive effects of TNF-alpha were due to specific activation of the HIV long terminal repeat, providing evidence that T NF-alpha may play a role in the mechanisms of pathogenesis of HIV infection.
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