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Updated: Jul 29, 2025
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
HIV infection and cardiovascular disease have both shared and distinct monocyte gene expression features: Women's
Juan Lin1, Erik Ehinger2, David B Hanna1
1Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, United States of America.
Insights
Persistent inflammation in HIV patients drives cardiovascular disease (CVD). Non-classical monocytes (NCM) and intermediate monocytes (IM) show altered gene expression, particularly with comorbid HIV and CVD, highlighting potential therapeutic targets.
Area of Science:
- Immunology
- Cardiovascular Disease Research
- HIV/AIDS Research
Background:
- Persistent inflammation is a key factor in developing cardiovascular disease (CVD) as an HIV-associated comorbidity.
- Innate immune cells, particularly monocytes, are significant drivers of inflammation in individuals with HIV.
- Understanding monocyte subsets' roles is crucial for managing HIV-associated CVD.
Purpose of the Study:
- To investigate the contribution of circulating non-classical monocytes (NCM) and intermediate monocytes (IM) to the host response in long-term HIV infection.
- To examine the role of these monocyte subsets in HIV-associated CVD.
- To analyze transcriptomic differences in monocytes based on HIV status and CVD presence.
Main Methods:
- Study included women with and without chronic HIV infection, with and without subclinical CVD (C), matched for key demographics.
- Transcriptomic features were assessed in isolated IM and NCM from peripheral blood mononuclear cells.
- Gene expression patterns were compared across four groups: H-C-, H+C-, H-C+, and H+C+.
Main Results:
- IM gene expression was minimally affected by HIV or CVD alone but showed a distinct signature with comorbid HIV/CVD, reversible with lipid-lowering treatment.
- NCM exhibited altered gene expression in women with HIV, regardless of CVD status.
- The most significant gene expression changes were observed in NCM from women with both HIV and CVD, with upregulated genes like LAG3 (CD223) identified as potential drug targets.
Conclusions:
- Circulating monocytes in well-controlled HIV infection display extensive gene expression signatures, potentially indicating their role as viral reservoirs.
- Gene expression alterations in HIV-positive individuals are amplified by the presence of subclinical CVD.
- These findings underscore the complex interplay between HIV, monocytes, and cardiovascular health, suggesting avenues for targeted therapies.
Abstract:
Persistent inflammation contributes to the development of cardiovascular disease (CVD) as an HIV-associated comorbidity. Innate immune cells such as monocytes are major drivers of inflammation in men and women with HIV. The study objectives are to examine the contribution of circulating non-classical monocytes (NCM, CD14dimCD16+) and intermediate monocytes (IM, CD14+CD16+) to the host response to long-term HIV infection and HIV-associated CVD. Women with and without chronic HIV infection (H) were studied. Subclinical CVD (C) was detected as plaques imaged by B-mode carotid artery ultrasound. The study included H-C-, H+C-, H-C+, and H+C+ participants (23 of each, matched on race/ethnicity, age and smoking status), selected from among enrollees in the Women's Interagency HIV Study. We assessed transcriptomic features associated with HIV or CVD alone or comorbid HIV/CVD comparing to healthy (H-C-) participants in IM and NCM isolated from peripheral blood mononuclear cells. IM gene expression was little affected by HIV alone or CVD alone. In IM, coexisting HIV and CVD produced a measurable gene transcription signature, which was abolished by lipid-lowering treatment. In NCM, versus non-HIV controls, women with HIV had altered gene expression, irrespective of whether or not they had comorbid CVD. The largest set of differentially expressed genes was found in NCM among women with both HIV and CVD. Genes upregulated in association with HIV included several potential targets of drug therapies, including LAG3 (CD223). In conclusion, circulating monocytes from patients with well controlled HIV infection demonstrate an extensive gene expression signature which may be consistent with the ability of these cells to serve as potential viral reservoirs. Gene transcriptional changes in HIV patients were further magnified in the presence of subclinical CVD.
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