Visceral leishmaniasis in a patient seropositive for HIV

Alvar, Jorge; Verdejo, J; Osuna, Antonio; Nájera, Rafael

doi:10.1007/bf02014266

Cited by 16 publications

(6 citation statements)

References 3 publications

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“…Recurrences of VL can be treated de novo with Sb V (10,20,243), for which reason an increase in the treatment time has been suggested. Nevertheless, the efficiency of this drug can decrease (81,113), perhaps because the parasite develops resistance to the drug (16,165). The efficiency of second-line treatments under these circumstances has not been adequately explored.…”

Section: Treatment Of Relapsesmentioning

confidence: 99%

Leishmania and human immunodeficiency virus coinfection: the first 10 years

et al. 1997

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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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Section: Treatment Of Relapsesmentioning

confidence: 99%

Leishmania and human immunodeficiency virus coinfection: the first 10 years

et al. 1997

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“…In particular, Leishmania organisms will rapidly become more important as pathogens in HIV-infected individuals, since the presence of Leishmania organisms is overlapping with the presence of HIV in several countries. The fact that Leishmania organisms are opportunistic in immunosuppressed patients, such as those infected with HIV (2,9), further reinforces this notion.…”

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confidence: 91%

Activation of human immunodeficiency virus type 1 in monocytoid cells by the protozoan parasite Leishmania donovani

Bernier

Turco

Olivier

et al. 1995

J Virol

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In this study, we demonstrated that the protozoan parasite Leishmania donovani and one of its major surface molecules, the lipophosphoglycan (LPG), can induce human immunodeficiency virus type 1 (HIV-1) expression in U1 and OM-10.1, two cell lines of monocytoid origin latently infected with HIV-1. Treatment of U1 cells with various concentrations of LPG (1, 5, and 10 M) resulted in a dose-dependent secretion of tumor necrosis factor alpha (TNF-␣). Suppression of LPG-induced HIV-1 expression by polyclonal anti-TNF-␣ antibodies further confirmed the involvement of this cytokine. Results from these studies indicate that the protozoan parasite L. donovani can induce the secretion of TNF-␣ that will function in an autocrine or paracrine manner to upregulate HIV-1 expression. Our data suggest for the first time that this protozoan parasite can be viewed as a potential cofactor in the pathogenesis of AIDS.

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“…Overall, it seems contradictory that LPG would inhibit HIV‐1‐mediated syncytium formation and viral entry when dual infection with HIV‐1 and Leishmania accelerates the progression of HIV‐1‐related diseases. In fact, Leishmania is suggested to be a potent cofactor for HIV‐1 replication and AIDS progression (reviewed in [75–77]). The reason for such a discrepancy probably stems from the fact that Leishmania /HIV−1 interactions are very complex, in part through their sharing of similar targets, namely cells of the mononuclear phagocyte series (i.e.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HIV-1-mediated syncytium formation and virus replication by the lipophosphoglycan fromLeishmania donovaniis due to an effect on early events in the virus life cycle

Genois

Barbeau

Olivier

et al. 2001

Clinical and Experimental Immunology

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Previous findings have indicated that the major surface molecule of Leishmania, lipophosphoglycan (LPG), could abrogate HIV‐1‐induced syncytium formation and virus replication. In the present work, we were interested in characterizing this inhibitory process. Data from a new luciferase‐based semiquantitative assay for syncytium formation, relying on the coincubation of a T‐cell line containing an HIV‐1 LTR‐driven luciferase construct with a cell line chronically infected with HIV‐1, confirmed that LPG was indeed a strong inhibitor of HIV‐1‐dependent syncytium formation and that this inhibition was dose‐dependent. As determined by flow cytometric analyses, this inhibition was not apparently due to downregulation of CD4, CXCR4 or LFA‐1, three distinct surface glycoproteins known to be important in HIV‐1 mediated syncytium formation. Furthermore, LPG did not seem to affect signal transduction pathways in T cells as judged by measurement of HIV‐1 LTR‐driven reporter gene activity upon treatment with different stimuli. However, pretreatment of either of the cell lines used in the assay with LPG led to a significant decrease of virus‐mediated syncytium formation, which was further accentuated when both cell lines were pretreated. LPG inhibition of HIV‐1 replication was next assessed. When measuring either infection with luciferase‐encoding recombinant HIV‐1 particles or multinucleated giant cell formation following an acute virus infection, we again observed that LPG was efficient at blocking HIV‐1 replication. Specific assays probing different steps of viral entry demonstrated that attachment was not hindered by LPG but that viral entry was modulated, suggesting that LPG targets a postbinding step. Hence, incorporation of LPG into a target cell membrane could influence its fluidity and diminish both the virus‐cell and cell‐to‐cell fusion processes initiated by HIV‐1.

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Visceral leishmaniasis in a patient seropositive for HIV

Cited by 16 publications

References 3 publications

Leishmania and human immunodeficiency virus coinfection: the first 10 years

Leishmania and human immunodeficiency virus coinfection: the first 10 years

Activation of human immunodeficiency virus type 1 in monocytoid cells by the protozoan parasite Leishmania donovani

Inhibition of HIV-1-mediated syncytium formation and virus replication by the lipophosphoglycan fromLeishmania donovaniis due to an effect on early events in the virus life cycle

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