ArticlePloS one2026
Cross-omics mapping of the human HIV restrictome across clinical states, immune-cell compartments, and protein responses.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host restriction factors can block HIV at multiple stages, but they are often studied as individual genes or within a single molecular layer. I performed an evidence-structured computational reanalysis of three independent public datasets to determine how the human HIV restrictome varies across clinical states, immune-cell compartments, and protein responses. The analysis used bulk monocyte RNA sequencing (GSE157198), PBMC single-cell/CITE-seq data (GSE256089), and primary CD4 T-cell proteomics (PXD012263) within a prespecified restrictome-immunometabolism framework. In GSE157198, ART-naive monocytes had higher core-restrictome activity than healthy controls (difference = 1.154, p = 0.000746), and core scores were strongly correlated with interferon/innate-sensing scores (Spearman r = 0.800, p = 7.47 × 10^-11). Core-lipid/cholesterol correlation was weaker and was not independent of interferon after conditional analysis. In GSE256089, participant-paired core-restrictome scores were enriched in NK cells relative to B cells, monocytes, and T cells, and matched random-gene-set analyses supported enrichment beyond background expression structure. FCGR3A monocytes also had higher participant-paired core scores than CD14 monocytes. Exploratory sensing/death-gene analysis identified cell-type-specific expression patterns but did not establish pathway activation, pyroptosis, or apoptosis. In PXD012263, the historical q < 0.05 proteomic selection contained 19 curated genes and retained mixed response polarity; sensitivity thresholds q < 0.01 and q < 0.10 selected 10 and 25 genes, respectively. Together, the results show that HIV restrictome activity varies across clinical and immune-cell contexts and is embedded within broader interferon-linked and immunometabolic states. Because the datasets are independent and not subject matched, the findings are observational and hypothesis-generating rather than causal.
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.