ArticleInfectious diseases of poverty2024
Investigation of parasite genetic variation and systemic immune responses in patients presenting with different clinical presentations of cutaneous leishmaniasis caused by Leishmania aethiopica.
Article in Infectious diseases of poverty, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- "It left me burnt": Traditional treatment and stigma experiences of cutaneous leishmaniasis in Kalu district, Ethiopia.PLoS neglected tropical diseases · 2026Article
- From dogma to data: charting a path forward for clinico-immunological research in Ethiopian cutaneous leishmaniasis.Infectious diseases of poverty · 2026Review
- Spatial mapping of Ethiopian cutaneous leishmaniasis lesions reveals distinct tissue level immune programs.Frontiers in immunology · 2026Article
- Molecular diagnostics for cutaneous leishmaniasis: progress towards fulfilling the WHO target product profile.Parasitology · 2025Review
- Genetic variation of cutaneous leishmaniasis causative species in Ethiopia.Scientific reports · 2025Article
- Ambiguities in cutaneous leishmaniasis classification and the need for consensus: Experience from Ethiopia.PLoS neglected tropical diseases · 2025Article
- Molecular epidemiology, distribution, and determinants of cutaneous leishmaniasis in Northeast Ethiopia.Scientific reports · 2025Article
- Cytokine Production in Response to Soluble Leishmania Aethiopica Antigen by Whole Blood Cells from Patients with Different Clinical Presentations of Cutaneous Leishmaniasis.The American journal of tropical medicine and hygiene · 2025Article
- Distinct neutrophil effector functions in response to different isolates of Leishmania aethiopica.Parasites & vectors · 2024Article
- Demographic characteristics and clinical features of patients presenting with different forms of cutaneous leishmaniasis, in Lay Gayint, Northern Ethiopia.PLoS neglected tropical diseases · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
backgroundCutaneous leishmaniasis (CL) is a neglected tropical skin disease, caused by the protozoan parasite Leishmania. In Ethiopia, CL is mainly caused by Leishmania aethiopica and can present in different clinical forms. The aim of this study was to assess whether these different forms are associated with differences in parasite genetic and host systemic immune signatures.
methodsHere we analysed the whole genome sequence data for 48 clinical parasite isolates and the systemic immune signature from a cohort of CL patients, who were recruited in Nefas Mewcha, Northern Ethiopia, from January 2019 to January 2022.
resultsOur results show that parasites from CL cases with different presentations in a single Ethiopian setting are from the same genetic population based on a permutation test of genome-wide similarity. Furthermore, a logistic regression test for genome wide association did not identify any individual genetic variants significantly associated with disease presentation. We also measured plasma chemokine and cytokine levels of 129 CL patients presenting with different forms of CL. None of the chemokine [eotaxin, eotaxin-3, interleukin (IL)-8, interferon (IFN)-γ-induced protein-10 (IP-10), monocyte chemoattractant protein (MCP)-1, MCP-4, macrophage-derived chemokines (MDC), macrophage inflammatory protein (MIP)-1α, MIP-1β and thymus- and activation-regulated chemokine (TARC)] or cytokine (IFN-γ, IL-1β, interleukin-2, IL-4, IL-6, IL-10, IL-12p70, IL-13, tumor necrosis factor-α) levels measured were significantly different between the different clinical presentations of CL, as measured by Kruskal-Wallis test. We also compared those with healthy nonendemic controls: our results show a chemokine (IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β and TARC) but not a cytokine immune signature in patients with CL as compared to healthy nonendemic controls, as measured by Mann-Whitney test.
conclusionsThe results of our study did not identify a systemic immune signature or parasite genetic factors associated with different clinical presentation of CL.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.