ArticlemBio2014
New clues to understanding HIV nonprogressors: low cholesterol blocks HIV trans infection.
Article in mBio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 13 citations in OpenAlex.
- Biophysics of Membrane Stiffening by Cholesterol and Phosphatidylinositol 4,5-bisphosphate (PIP2).Advances in experimental medicine and biology · 2023Article
- Cholesterol Stiffening of Lipid Membranes.The Journal of membrane biology · 2022Review
- How cholesterol stiffens unsaturated lipid membranes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Comorbidities of HIV infection: role of Nef-induced impairment of cholesterol metabolism and lipid raft functionality.AIDS (London, England) · 2020Review
- HIV-1 viral protein R (Vpr) induces fatty liver in mice via LXRα and PPARα dysregulation: implications for HIV-specific pathogenesis of NAFLD.Scientific reports · 2017Article
- Cellular Cholesterol Facilitates the Postentry Replication Cycle of Herpes Simplex Virus 1.Journal of virology · 2017Article
- Cholesterol-conjugated peptide antivirals: a path to a rapid response to emerging viral diseases.Journal of peptide science : an official publication of the European Peptide Society · 2015Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
A small percentage of HIV-infected subjects (2 to 15%) are able to control disease progression for many years without antiretroviral therapy. Years of intense studies of virologic and immunologic mechanisms of disease control in such individuals yielded a number of possible host genes that could be responsible for the preservation of immune functions, from immune surveillance genes, chemokines, or their receptors to anti-HIV restriction factors. A recent mBio paper by Rappocciolo et al. (G. Rappocciolo, M. Jais, P. Piazza, T. A. Reinhart, S. J. Berendam, L. Garcia-Exposito, P. Gupta, and C. R. Rinaldo, mBio 5:e01031-13, 2014) describes another potential factor controlling disease progression: cholesterol levels in antigen-presenting cells. In this commentary, we provide a brief background of the role of cholesterol in HIV infection, discuss the results of the study by Rappocciolo et al., and present the implications of their findings.
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.