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Updated: Sep 9, 2025
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
EcoHIV Infection Promotes Atherosclerosis Progression in LDLR-Deficient Mice
Ivan Pinos1, Amparo Blanco1, Jennifer Kelschenbach2
1Division of Nutritional Sciences (I.P., A.B., J.A.), University of Illinois Urbana-Champaign.
Insights
This study reveals how HIV infection impacts cardiovascular disease using a mouse model. EcoHIV infection in mice mimics human immunodeficiency virus-associated atherosclerosis, offering insights for new treatments.
Area of Science:
- Cardiovascular Science
- Virology
- Immunology
Background:
- People with HIV face increased risk of atherosclerotic cardiovascular disease (ASCVD).
- Molecular mechanisms linking HIV and ASCVD are poorly understood.
- Lack of suitable animal models hinders research.
Purpose of the Study:
- To investigate the impact of HIV on ASCVD pathogenesis.
- To establish a relevant animal model for HIV-associated cardiovascular disease.
- To explore molecular changes in atherosclerosis due to HIV infection.
Main Methods:
- Infection of atheroprone low-density lipoprotein receptor-deficient (Ldlr-/-) mice with chimeric HIV (EcoHIV).
- Analysis of inflammatory monocyte markers, recruitment, and lesion composition.
- Assessment of lesion vulnerability, necrotic core size, and collagen content.
Main Results:
- EcoHIV infection increased inflammatory monocytes and their recruitment to lesions.
- Lesions showed increased vulnerability, larger necrotic cores, and reduced collagen.
- Active EcoHIV replication was observed within atherosclerotic lesions.
- These changes occurred independently of plasma lipid profiles or lesion size.
Conclusions:
- EcoHIV infection in Ldlr-/- mice effectively models HIV-associated ASCVD.
- Findings highlight potential therapeutic targets for cardiovascular complications in people with HIV.
- This model provides a platform for developing interventions for HIV-infected individuals at high cardiovascular risk.
Background:
People with HIV are at higher risk of atherosclerotic cardiovascular disease than uninfected individuals; however, the molecular mechanisms behind this association remain elusive due to the lack of suitable animal models.
Methods:
To study the impact of HIV on atherosclerotic cardiovascular disease, we infected the atheroprone Ldlr-/- mice with the chimeric virus EcoHIV.
Results:
In comparison to uninfected controls, EcoHIV infection increased the ratio of circulating inflammatory monocytes, monocyte recruitment, and CD68+ content in the atherosclerotic lesion. These changes occurred independently of alterations in plasma lipid profile or lesion size between groups. Lesions of EcoHIV-infected mice displayed greater vulnerability to rupture, as determined by increased necrotic core area and CD38+ content, and reduced presence of collagen compared with uninfected mice. Last, we report the presence of active viral replication of EcoHIV in the atherosclerotic lesion.
Conclusions:
Our data suggest that EcoHIV infection in Ldlr-/- mice resembles the pathogenesis of atherosclerotic cardiovascular disease in people with HIV. Our findings have therapeutic implications for people with HIV, a vulnerable population with an elevated risk of cardiovascular disease.
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