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Mouse Models of HIV-Associated Atherosclerosis
Victoria R Stephens1,2, Sharareh Ameli1,3,4, Amy S Major1,3,4,5
1Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Insights
Cardiovascular disease (CVD) remains a leading cause of death. Advanced mouse models are crucial for understanding HIV-associated atherosclerosis and immune mechanisms driving CVD, especially when traditional statin therapy falls short.
Area of Science:
- Immunology
- Cardiovascular Science
- Infectious Disease
Background:
- Cardiovascular disease (CVD) is the primary global cause of mortality.
- People living with HIV (PLWH) face double the risk of CVD compared to HIV-negative individuals.
- Despite statin therapy and antiretroviral treatment (ART), PLWH exhibit persistent inflammation, a key driver of CVD.
Purpose of the Study:
- To summarize atherosclerosis development and review mouse models for studying HIV-associated atherosclerosis.
- To highlight the limitations of current statin therapies in reducing CVD prevalence in PLWH.
- To emphasize the need for advanced methodologies in studying HIV-associated CVD.
Main Methods:
- Review of existing literature on atherosclerosis pathogenesis and mouse models.
- Discussion of dietary and genetic manipulations used to create atheroprotective mouse models.
- Evaluation of integrating multi-omics, genetic engineering, and immune cell profiling in mouse models.
Main Results:
- Most mouse strains possess inherent atheroprotective mechanisms, necessitating tailored models for CVD research.
- HIV-associated atherosclerosis requires specialized mouse models that mimic human disease conditions.
- Advanced approaches like multi-omics and immune profiling enhance the study of CVD mechanisms in HIV.
Conclusions:
- Mouse models are essential for dissecting the complexities of atherosclerosis, particularly in the context of HIV.
- Integrating multi-omics, genetic manipulation, and immune profiling in mouse models offers powerful tools to study HIV-associated CVD.
- These advanced methods are vital for addressing knowledge gaps in the immune mechanisms underlying CVD in PLWH.
Abstract:
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Several factors are implicated in the pathogenesis of CVD, and efforts have been made to reduce traditional risks, yet CVD remains a complex burden. Notably, people living with HIV (PLWH) are twice as likely to develop CVD compared to persons without HIV (PWoH). Intensive statin therapy, the first-line treatment to prevent cardiovascular events, is effective at reducing morbidity and mortality. However, statin therapy has not reduced the overall prevalence of CVD. Despite antiretroviral therapy (ART), and new guidelines for statin use, PLWH have persistent elevation of inflammatory markers, which is suggested to be a bigger driver of future cardiovascular events than low-density lipoprotein. Herein, we have summarized the development of atherosclerosis and highlighted mouse models of atherosclerosis in the presence and absence of HIV. Since most mouse strains have several mechanisms that are atheroprotective, researchers have developed mouse models to study CVD using dietary and genetic manipulations. In evaluating the current methodologies for studying HIV-associated atherosclerosis, we have detailed the benefits of integrating multi-omics analyses, genetic manipulations, and immune cell profiling within mouse models. These advanced approaches significantly enhance our capacity to address critical gaps in understanding the immune mechanisms driving CVD, including in the context of HIV.
