ArticleFrontiers in immunology2026
Unsupervised proteomic stratification of people living with HIV reveals inflammatory biotypes beyond conventional clinical classifications.
Article in Frontiers in immunology, 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
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Conventional HIV-1 management relies on clinical phenotypes, assuming a uniform inflammatory status and overlooking biological heterogeneity. We aimed to employ a high-throughput proteomic approach to stratify people living with HIV (PLWH) based on plasma inflammatory profiles and evaluate their association with comorbidity burden. Methods: This cross-sectional study included 30 PLWH (10 treatment-naïve, 10 ART-suppressed, and 10 elite controllers (EC)) and 10 seronegative controls. Unsupervised hierarchical clustering was applied to 87 inflammatory proteins (analyzed by proximity extension assay and ELISA). A Random Forest model stabilized with 1,000 trees identified the variables defining the biotypes. Comorbidity burden was assessed within the virally suppressed groups (ART-suppressed and EC). Results: Clustering revealed two distinct biological profiles independent of clinical classifications: a high-inflammation biotype (n=11) and a low-inflammation biotype (n=19). Within the treatment-naïve, elite controller, and ART-suppressed groups, 60%, 30%, and 20% of participants, respectively, were classified as belonging to the high-inflammation biotype. PDL1, CD40, TNF, LAP-TGFbeta1, and SLAMF1 were the top biological drivers of this separation. A trend for a higher comorbidity burden was observed in the high-inflammation biotype compared to the low-inflammation group (p=0.06). Conclusions: Plasma inflammatory profiling stratifies PLWH into distinct biological biotypes that bypass conventional classifications. The observed differences in comorbidity burden between inflammatory biotypes warrant further investigation in larger prospective studies to clarify their clinical relevance and potential implications for long-term health outcomes.
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.