ReviewCellular and molecular life sciences : CMLS2018
Control of HIV infection by IFN-α: implications for latency and a cure.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 21 citations in OpenAlex.
- IFI27 inhibits HIV-1 replication by degrading Gag protein through the ubiquitin-proteasome pathway.Journal of virology · 2024Article
- Role of Type I Interferons duringBiomolecules · 2024Review
- Mechanisms underlying HIV-associated cognitive impairment and emerging therapies for its management.Nature reviews. Neurology · 2023Review
- Genetic polymorphisms in thePeerJ · 2023Article
- MX2 Viral Substrate Breadth and Inhibitory Activity Are Regulated by Protein Phosphorylation.mBio · 2022Article
- The role of IFN-γ production during retroviral infections: an important cytokine involved in chronic inflammation and pathogenesis.Revista do Instituto de Medicina Tropical de Sao Paulo · 2022Review
- An HIV elite controller patient carrying the homozygous H63D variant in the homeostatic iron regulator gene: A case report.Medicine · 2021Article
- MX2-mediated innate immunity against HIV-1 is regulated by serine phosphorylation.Nature microbiology · 2021Article
- Identification of Latent Diagnostic Biomarkers and Biological Pathways in Dermatomyositis Based on WGCNA.Journal of oncology · 2021Article
- HBV/HIV Coinfection: Impact on the Development and Clinical Treatment of Liver Diseases.Frontiers in medicine · 2021Review
- The Role of Dendritic Cells During Infections Caused by Highly Prevalent Viruses.Frontiers in immunology · 2020Review
- HIV-1 Promotes the Degradation of Components of the Type 1 IFN JAK/STAT Pathway and Blocks Anti-viral ISG Induction.EBioMedicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Viral infections, including HIV, trigger the production of type I interferons (IFNs), which in turn, activate a signalling cascade that ultimately culminates with the expression of anti-viral proteins. Mounting evidence suggests that type I IFNs, in particular IFN-α, play a pivotal role in limiting acute HIV infection. Highly active anti-retroviral treatment reduces viral load and increases life expectancy in HIV positive patients; however, it fails to fully eliminate latent HIV reservoirs. To revisit HIV as a curable disease, this article reviews a body of literature that highlights type I IFNs as mediators in the control of HIV infection, with particular focus on the anti-HIV restriction factors induced and/or activated by IFN-α. In addition, we discuss the relevance of type I IFN treatment in the context of HIV latency reversal, novel therapeutic intervention strategies and the potential for full HIV clearance.
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.