People living with HIV-1 (PWH) who are receiving antiretroviral therapy (ART) continue to experience an increased risk of cardiovascular disease (CVD) compared with people without HIV. Coronary atherosclerotic plaque formation in this population has been associated with chronic immune activation. Proposed drivers of persistent immune activation during ART include residual HIV-1 production and microbial translocation from the gut.
The authors' prior work identified that aldehyde dehydrogenase (ALDH), the enzyme that converts vitamin A into retinoic acid (RA), is upregulated in myeloid cells after exposure to viral, bacterial, or fungal products, and that RA promotes HIV-1 production. These observations motivated investigation of a possible link between the ALDH/RA metabolic pathway in myeloid cells and CVD risk in ART-treated PWH.
The study used peripheral blood mononuclear cells (PBMCs) and plasma collected from two groups: ART-treated people with HIV-1 (PWH+ART; n=51) and people without HIV-1 (Pw/oH; n=63). Samples were drawn from the Ca cohort referenced in the preprint. The source text provided here is truncated and does not report additional cohort characteristics such as age distribution, sex, cardiovascular risk factors, ART regimens, or duration of HIV infection and ART.
ALDH enzymes catalyze the oxidation of retinaldehyde to retinoic acid (RA), a biologically active metabolite of vitamin A. In previous studies cited by the authors, exposure of myeloid cells to microbial or viral stimuli induced ALDH expression. The same prior work indicated that RA can enhance HIV-1 production, suggesting a mechanistic intersection between innate immune activation, vitamin A metabolism, and viral persistence.
The principal aim described in the abstract was to explore the relationship between the ALDH/RA pathway in monocytes/myeloid cells and the risk of coronary atherosclerosis in ART-treated PWH. The study evaluated PBMC and plasma samples from PWH+ART and from people without HIV to address this question.
The abstract specifies use of PBMCs and plasma from the two groups (PWH+ART; n=51 and Pw/oH; n=63). Beyond sample sources and group sizes, the excerpted source does not include detailed methodological information. Specifically, the following were not reported in the available text:
Because these details are missing from the provided excerpt, they could not be summarized here and must be obtained from the full preprint or subsequent peer-reviewed publication.
The abstract states the overarching finding in its title and opening sentences: ALDH activity in monocytes is associated with subclinical coronary atherosclerosis in treated people with HIV-1. The truncated source excerpt does not provide granular results—numerical values, measures of association, confidence intervals, or p-values are not present in the text supplied. Likewise, specific differences between PWH+ART and Pw/oH groups, or whether plasma RA levels or monocyte ALDH expression correlated with imaging or biomarker measures of plaque, are not reported in the available excerpt.
From the information provided, the study links a metabolic pathway in myeloid cells—ALDH-mediated production of retinoic acid—to subclinical coronary atherosclerosis in ART-treated PWH. If supported by full methods and data, this would suggest a potential mechanism by which immune activation and vitamin A metabolism intersect with HIV-related cardiovascular risk. It raises the possibility that ALDH/RA signaling in monocytes could serve as a biomarker or a mechanistic target for interventions aimed at reducing CVD risk in this population. However, the degree of association, causality, and clinical relevance cannot be judged from the truncated abstract alone.
The preprint reports an association between monocyte ALDH activity and subclinical coronary atherosclerosis in ART-treated people with HIV-1, based on analysis of PBMCs and plasma from PWH+ART and control participants. The abstract provides rationale linking chronic immune activation, ALDH induction in myeloid cells, and RA-mediated effects on HIV-1 production. Full evaluation of the study’s validity and implications requires the complete methods, result tables, and statistical analyses, which were not included in the excerpted source material presented here.
References and further details were not reported in the provided source excerpt; readers should consult the full preprint (doi: https://doi.org/10.64898/2026.08.20.746037) and subsequent peer-reviewed publications for complete data and methodological information.