ArticleCurrent trends in immunology2016
Defective iron homeostasis in human immunodeficiency virus type-1 latency.
Article in Current trends in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Contemporary Antiretroviral Therapy Dysregulates Iron Transport and Augments Mitochondrial Dysfunction in HIV-Infected Human Microglia and Neural-Lineage Cells.International journal of molecular sciences · 2023Article
- HIV-1 infection in sickle cell disease and sickle cell trait: role of iron and innate response.Expert review of hematology · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Highly active antiretroviral therapy has significantly improved the life of HIV-1-infected individuals, yet complete eradication of HIV-1 reservoirs (i.e., latently infected cells) remains a major challenge. We have previously shown that induction of the endogenous cytoprotective enzyme heme oxygenase-1 (HO-1) by its natural substrate hemin reduces susceptibility of T cells and macrophages to HIV-1 infection. In the present study, we demonstrate that hemin treatment stimulated virus production by latently infected ACH-2 cells, followed by cellular toxicity and death when stimulated with TNF-α or co-cultured with monocyte-derived macrophages (MDM). This cytotoxicity was associated with low levels of the iron-binding protein ferritin and the iron transporter ferroportin with lack of hemoglobin catabolic enzyme HO-1, resulting in substantial iron accumulation in the activated ACH-2 cells. Defective iron homeostasis in ACH-2 cells provides a model system for selective targeting of the latent HIV-1 reservoir by hemin-induced iron toxicity.
Indexed as
Identifiers
28824260PMC5562369W2965573127What 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.