The Kovacs laboratory focuses on investigating the mechanistic links between HIV and pulmonary vascular disease (PVD) while identifying the molecular mechanisms through which HIV-derived proteins contribute to the pathological processes of HIV-associated pulmonary vascular remodeling and cardiopulmonary alterations. My research program uses mouse models of HIV and smooth muscle-specific knockout (KO) mouse models to explore the signaling pathways involved in HIV-related PVD. We utilize echocardiography, hemodynamic measurements, and morphometric analysis to assess pulmonary arterial remodeling, PVD, and right ventricular hypertrophy (RVH), along with in vitro molecular biology approaches in primary isolated vascular smooth muscle cells to dissect the underlying molecular mechanisms involved in these processes. Our long-term goal is to develop new therapeutic strategies for the intervention and treatment of HIV-associated cardiopulmonary complications.
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The introduction of combination antiretroviral therapy (cART) has led to a dramatic suppression of HIV replication and improved the lifespan of people with HIV (PWH), which now approaches that of the general population.
Although effective HIV treatments have dramatically decreased HIV/AIDS-related mortality, cardiovascular disease has become the leading cause of death in PWH.
PWH suffers from a higher risk of pulmonary vascular disease (PVD), the prevalence of which is more than 8 times higher in PWH than in HIV negative individuals. PVD is amongst the most devastating cardiovascular complications of HIV.
My primary research goals are to investigate:
Schematic figure shows the potential mechanisms in which HIV infection, viral proteins, and combination antiretroviral therapy (cART) contribute to endothelial dysfunction leading to HIV-associated cardiovascular disease. (Kovacs L, et al., J Am Coll Cardiol Basic Trans Science. 2022;7(4):410鈥�421
