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Use of the transgenic mouse in models of AIDS cardiomyopathy
1Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA. wlewis@emory.edu
Insights
Heart disease in acquired immunodeficiency syndrome (AIDS) involves complex factors. Transgenic mice models help define how HIV-1 gene products impact heart function and structure.
Area of Science:
- Cardiology
- Virology
- Genetics
Background:
- Heart disease, particularly cardiomyopathy (CM), is a growing concern in AIDS patients.
- The exact causes of AIDS CM are not fully understood, with potential factors including HIV-1 infection, opportunistic infections, inflammation, cytokines, and drug toxicity.
- Multiple factors likely contribute to the development of CM in AIDS.
Purpose of the Study:
- To investigate the pathogenetic mechanisms of AIDS-related cardiomyopathy (CM).
- To utilize transgenic mouse (TG) models to study the effects of HIV-1 gene products on cardiac myocytes.
- To define the cardiovascular effects of AIDS and its therapy on heart structure and function.
Main Methods:
- Employing transgenic mice (TG) models that express HIV-1 gene products.
- Utilizing both targeted and non-targeted TG to study specific HIV-1 gene effects.
- Developing cardiac-specific TG for ventricular myocyte expression of selected HIV-1 genes.
- Combining in vivo and in vitro studies in AIDS models.
Main Results:
- Transgenic mice models provide a platform to elucidate AIDS CM mechanisms.
- Targeted TG allow for the study of structural and functional effects of specific HIV-1 gene products on heart tissue.
- This approach enables the definition of environmental agents' impact, including cardiotoxins.
Conclusions:
- Transgenic mice are valuable tools for understanding AIDS CM.
- Tissue-specific targeting of HIV-1 genes in cardiac myocytes is crucial for defining their effects.
- This research models the clinical condition to understand cardiovascular effects of AIDS and its treatment.
Abstract:
Heart disease in AIDS, particularly cardiomyopathy (CM), is an increasingly recognized clinical problem with as yet undefined pathogenetic mechanisms. Among the potential etiologies of AIDS CM are HIV-1 infection of cardiac myocytes and subsequent cardiac dysfunction, opportunistic infection, inflammatory reactions, cytokine effects, and cardiotoxicity of prescribed or illicit drugs. It seems probable that multiple factors may impact on the development of CM in AIDS. Transgenic mice (TG) are useful biological tools to explore mechanisms of cardiac function and disease. In AIDS models, TG offer novel ways to elucidate mechanisms of AIDS CM through combined in vivo and in vitro studies. With targeted and non-targeted TG, structural and functional effects of specific HIV-1 gene products on heart tissue may be addressed. The impact of environmental agents including therapeutics or cardiotoxins may also be defined. To address the complexity of AIDS CM using TG, an experimental approach has been employed in our laboratories to model the clinical condition. We utilize AIDS TG with generalized expression of HIV-1 gene products in CM models with combined antiretroviral regimens to define the cardiovascular effects of AIDS and its therapy on the structure and function of the murine heart. We are developing a series of cardiac specific TG bearing selected HIV-1 genes. These TG target the selected HIV-1 genes expressed in cardiac ventricular myocytes. Tissue-specific targeting of this type enables us to define structural and functional effects of specific HIV-1 gene products on the cardiac myocyte.
